The Murphy et al. letter1 is notable for its ad hominem claims, the first of which comes in their introductory remarks. Noting that my review2 reports no conflicts of interest, they make the exaggerated claim that I have “written extensively on the ‘lethality’ of caffeine”. That claim cites one published article, titled “Death by Caffeine”,3 which summarises reports of death by poisoning involving documented cases from coronial and other official public inquiries. As reported in that article, official records in several countries report multiple confirmed cases of death by poisoning due to caffeine. Although relatively rare, such cases have been (and continue to be) reported worldwide. Predicated on the mere fact that I have previously reported findings from official inquiries into caffeine-related harm, the claim by Murphy et al. of “conflict” is perverse. By implication, their reasoning would mean that the reporting of harm from any source (which includes much of the content of medical journals) renders authors (i.e., most medical researchers) evermore vulnerable to bias warranting formal disclosure of conflict of interest in all future reports on the same or related topic. Of course, no such custom or practice exists.
Notably, the assertion of conflict in this instance indicates poor understanding of the matter, a lamentable situation considering the professional identities of Murphy and her 20 co-authors. Conflict of interest arises when a primary interest conf...
The Murphy et al. letter1 is notable for its ad hominem claims, the first of which comes in their introductory remarks. Noting that my review2 reports no conflicts of interest, they make the exaggerated claim that I have “written extensively on the ‘lethality’ of caffeine”. That claim cites one published article, titled “Death by Caffeine”,3 which summarises reports of death by poisoning involving documented cases from coronial and other official public inquiries. As reported in that article, official records in several countries report multiple confirmed cases of death by poisoning due to caffeine. Although relatively rare, such cases have been (and continue to be) reported worldwide. Predicated on the mere fact that I have previously reported findings from official inquiries into caffeine-related harm, the claim by Murphy et al. of “conflict” is perverse. By implication, their reasoning would mean that the reporting of harm from any source (which includes much of the content of medical journals) renders authors (i.e., most medical researchers) evermore vulnerable to bias warranting formal disclosure of conflict of interest in all future reports on the same or related topic. Of course, no such custom or practice exists.
Notably, the assertion of conflict in this instance indicates poor understanding of the matter, a lamentable situation considering the professional identities of Murphy and her 20 co-authors. Conflict of interest arises when a primary interest conflicts with a secondary interest.4,5 Examples of healthcare primary interests include researcher interest in producing generalisable knowledge, educator interest in sharing impartial knowledge, and healthcare personnel interest in delivering effective care. The quintessential example of secondary interest requiring disclosure is potential financial gain. However, disclosure is also required in such circumstances as affiliation with a stakeholder where such association could serve a secondary interest even when direct financial reward is not involved. We have no such affiliations, and our studies of caffeine, including caffeine and pregnancy,6 do not generate income.
Echoing sentiments held by O’Connor7 and Fernando,8 Murphy et al. claim that because my article2 is a narrative review, it falls “short of the standards”. In reality, it is common knowledge that all methods of scientific review possess particular advantages and disadvantages. In common with all scientific enterprise (including theoretical and empirical endeavours), each instance of scientific review should be assessed on its merits. The fact that much of the published literature examined in my review is in the form of systematic reviews and meta-analyses contributed to the choice of narrative review in this instance. Given the inconsistency between persistent claims of safety, on one hand, and extensive reports from prior quantitative syntheses of significant caffeine-related negative pregnancy outcomes on the other, there was need for the quantitative literature to be synthesised conceptually by way of “traditional” or narrative review. The claim by Murphy et al. of inherent superior objectivity for one or other review approach over legitimate alternatives reveals poor understanding of review practice and tradition.
Murphy et al. also claim that the articles examined in my review may not be “an unbiased reflection of the literature”. However, the review is transparent with respect to source material, and anyone concerned about selection bias is free to identify additional material. Murphy et al.’s belief that such material exists, despite no attempt by them to identify it, could itself be suggestive of bias. A litany of complaints then follows, wherein Murphy et al. express views contrary to those argued in the review. In particular, while it is (in their words) “clear that caffeine intake is associated with a higher risk of adverse pregnancy outcome”, Murphy et al. nevertheless seem unwilling to consider the implications of that reality. Oddly, they engage in ad hominem generalisations about confounding/misclassification and evidence of causation, when much of the review addresses those very issues in detail.
Under the heading “recommendations” and “lived” experience, Murphy et al. draw attention to concerns about the potential for information such as that reported in the review to cause distress, especially among women who have experienced a negative pregnancy outcome. This is a dilemma of real concern demanding calm and sensitive attention. Murphy et al.’s proselytising does not treat that dilemma with the calmness and sensitively it deserves, nor is the complex multifaceted nature of the dilemma given due consideration. While it is undeniably important that anxiety and guilt be avoided where possible, it is equally important not to withhold inconvenient information, especially information that could assist women in avoiding preventable harm. Thus, it is obviously appropriate to address anxiety or guilt women may feel on receipt of potentially disturbing new information. Likewise, it is important that appropriate support be given in the event of anger and anxiety being triggered when women learn of the failure by relevant authorities to give due prominence to long-held suspicions about caffeine-related harm.
Unfortunately, the contribution of moderate caffeine consumption to negative pregnancy outcomes does not leave an indelible footprint in its wake. Thus, for those who have experienced a negative pregnancy outcome, it is important to stress that caffeine could be but one of a plethora of potential contributing factors. There is simply no basis for making a specific assessment about the possible contribution of caffeine at the level of the individual case. It is equally important, however, to understand that whereas caffeine-related increased risk of harm is small at the level of each individual, that small increased risk when aggregated across populations is demonstrably not trivial,9 as evidenced by the many articles examined in our review.2 Geoffrey Rose, the eminent British epidemiologist, expressed the relevant principle well when he stated, “A population-wide preventive measure [in this instance, avoidance of caffeine during pregnancy] may offer a disappointingly trivial benefit to individuals, but yet its cumulative benefit for the population as a whole can be unexpectedly large” (pp. 102).10
Sadly, Murphy et al. falsely state that the review contains a “claim that 280,000 of the approximately 1 million miscarriages that take place in the USA each year are attributable to maternal caffeine consumption”. The claim appears to be a deliberate misreading of a table in an earlier version of the review. The earlier version (which I decided to amend) included a table (Table 3) predicated on a series of assumptions that included a hypothetical scenario about possible implications were all pregnant women to consume the recommended “safe” level of 200 mg caffeine per day (which the review posited as a purely theoretical, and unlikely, occurrence). However, it was apparent from early reader comment that speculation based on a hypothetical scenario, overtly intended merely to illustrate a point of principle, was potentially confusing and risked diverting some reader attention away from key evidence-based conclusions in the review. Accordingly, I deleted the content describing hypotheticals from the final version. Murphy et al.’s attempt to discredit the review by misreporting material that had been formally withdrawn seems to vindicate the decision to omit that content. However, it is important to note that inclusion or omission of the aforementioned theoretical argument has no bearing whatever on the conclusions, which remain entirely unaltered in both the earlier and amended (i.e., current) version of the manuscript.
Expressing a novel objection, Murphy et al. suggest that the conclusions of the review are “irresponsible” because women are incapable of avoiding caffeine. In that context, it is important to note that caffeine is a psychoactive substance and that repeated exposure leads to physical dependence.11,12 At the same time, it is equally important to understand that the addictive potential of caffeine is less than that of classic drugs of abuse (e.g., alcohol, amphetamines, cocaine, opioids). Indeed, relevant empirical research shows that simple and effective strategies are available to enable those who desire to reduce or eliminate caffeine consuming habits to succeed in so doing.13-15 The terms “avoid” and “eliminate” in this context refer to caffeine beverages (coffee, tea, so-called “energy” drinks, etc.) which account for almost all of the caffeine that is regularly consumed.
Caffeine at considerably lower concentrations is also contained in decaffeinated coffee and tea, hot chocolate, chocolate bars, chocolate confectionaries, and chocolate cake. Combined, those sources account for a trivial proportion of the total caffeine consumed worldwide, and are not the targets of the avoidance advice contained in our review. It is unclear why Murphy et al. prejudge pregnant women as incapable of avoiding caffeine. A more constructive approach would be to promulgate evidence-based findings and invite women to decide for themselves whether to expose their unborn child to a psychoactive drug, albeit one that is currently widely used, or to have, as far as is possible, a drug-free pregnancy.
To repeat key points from the review:2 chronic chemical exposure during pregnancy is always cause for concern; there is undisputed high biological plausibility of harm from caffeine consumed during pregnancy; there is consistent evidence of harm from diverse animal experiments, human observational studies, systematic reviews, and meta-analyses; findings are robust to threats form confounding and misclassification; caffeine has no nutritional benefit for either mother or baby; and persons wishing to reduce or eliminate dietary caffeine can do so successfully when shown how. Those and other realities provide compelling grounds for questioning the soundness of current advice about the reputed safety of “moderate” caffeine consumption during pregnancy.
Finally, while there is no reason to question good intentions, the emotional tone of the Murphy et al. letter and their fervent belief in the correctness of their views (despite current realities as summarised in the preceding paragraph), bear the hallmarks of a common cognitive bias, well-known to social psychology as self-serving bias. Extensive experimentation shows that human decision making is subject to an unintentional and unconscious self-serving bias, wherein reason and judgment are skewed in favour of outcomes in which the individual has a prior stake.16 It is reasonable to assume that most, if not all, of Murphy and her 20 co-authors are habitual caffeine consumers, sharing common features with other consumers, including physical dependence and desire to continue to consume. The self-serving bias therein is likely to encourage resistance to information that challenges habit. Absent of sound argument to reject the challenge, strong emotion and fervent belief typically come to the fore. Such reactions are understandable but regrettable. The public’s stake in women’s health is of a magnitude that calls for calm reflection and preparedness for sober engagement with the evidence concerning caffeine-related negative pregnancy outcomes.
References
1. Murphy C, Brown T, Trickey, H, et al. It remains unclear whether caffeine causes adverse pregnancy outcomes; but naive policy recommendations could cause harm. Evid Based Med 2020. Available: https://ebm.bmj.com/content/early/2020/09/01/bmjebm-2020-111432.responses.
2. James E. Maternal caffeine consumption and pregnancy outcomes: A narrative review with implications for advice to mothers and mothers-to-be. Evid Based Med 2020;25. Available: doi.org/10.1136/bmjebm-2020-111432.
3. James JE. Death by caffeine: How many caffeine-related fatalities and near–misses must there be before we regulate? J Caffeine Res 2012;2:149-152.
4. Relman AS. Dealing with conflicts of interest. N Engl J Med 1984;310:1182-3.
5. James JE. Disclosing conflict of interest does not mitigate healthcare bias and harm: It is time to sever industry ties. Eur J Clin Invest 2020;50, doi.org/10.1111/eci.13344.
6. James JE, Paull I. Caffeine and human reproduction. Rev Environ Health 1985;5:151–67.
7. James JE. Caffeine and Pregnancy: Bias? Is the pot calling the kettle black? Reply to O'Connor. Evid Based Med 2020;25.
8. James JE. Caffeine and pregnancy: Don’t shoot the messenger, please. Reply to Fernando. Evid Based Med 2020;25.
9. James JE. The health of populations. London: Elsevier-Academic Press, 2016
10. Rose G. The strategy of preventive medicine. Oxford, UK: Oxford University Press, 1992.
11. Griffiths RR, Juliano LM, Chausmer AL. Caffeine: pharmacology and clinical effects. In: Graham AW, Schultz TK, Mayo- Smith MF, Ries RK, Wilford BB (eds) Principles of addiction medicine, 3rd edn. (pp 134–193). Chevy Chase, MD: American Society of Addiction Medicine, 2003.
12. James JE, Rogers PJ. Effects of caffeine on performance and mood: Withdrawal reversal is the most plausible explanation. Psychopharmacol 2005;182:1-8.
13. Foxx RM, and Rubinoff, A. Behavioral treatment of caffeinism: reducing excessive coffee drinking. J App Behav.Anal. 1979;12:344-55.
14. James JE, Stirling K P, Hampton BAM. Caffeine fading: behavioral treatment of caffeine abuse. Behav Ther 1979;16:15-27.
15. James JE, Paull I, Cameron-Traub E, et al. Biochemical validation of self-reported caffeine consumption during caffeine fading. J Behav Med 1988;11:15-30.
16. Dana J, Loewenstein, G. A social science perspective on gifts to physicians from industry. JAMA 2003; 290:252–5.
Drs Clure and Lazorwitz have misunderstood and misinterpreted the Yellow Card data that we adduced to test the null hypothesis that there is no interaction of antibiotics with hormonal contraceptives. Here we reply to their specific comments.
“The medications in each group are not equivalent and bias the sample” We chose a wide range of medicines in order to minimize this. Clure and Lazorwitz have selected only two examples each from the group of nine control drugs and the group of nine non-enzyme-inducing antibiotics, and assert that the age distribution favours older women in the control group. However, they ignore the fact that the same could be asserted of the enzyme-inducing drugs, some of which are more likely to be used in older women, but had an even bigger effect than the antibiotics.
“The rates of unintended pregnancy reported … are much lower than expected in general users of oral contraception” This is an important misunderstanding, which we sought to obviate in the paper, by making it clear that the data do not allow calculation of the absolute rates of unintended pregnancies. That is because the reported rates are not rates of unintended pregnancies in women taking hormonal contraceptives, but the frequencies of reports of unintended pregnancies as a proportion of all reports of suspected adverse reactions. It is the ratios of frequencies that are important. In other words, whatever the baseline risk is, the risk is 13 times higher with enzyme i...
Drs Clure and Lazorwitz have misunderstood and misinterpreted the Yellow Card data that we adduced to test the null hypothesis that there is no interaction of antibiotics with hormonal contraceptives. Here we reply to their specific comments.
“The medications in each group are not equivalent and bias the sample” We chose a wide range of medicines in order to minimize this. Clure and Lazorwitz have selected only two examples each from the group of nine control drugs and the group of nine non-enzyme-inducing antibiotics, and assert that the age distribution favours older women in the control group. However, they ignore the fact that the same could be asserted of the enzyme-inducing drugs, some of which are more likely to be used in older women, but had an even bigger effect than the antibiotics.
“The rates of unintended pregnancy reported … are much lower than expected in general users of oral contraception” This is an important misunderstanding, which we sought to obviate in the paper, by making it clear that the data do not allow calculation of the absolute rates of unintended pregnancies. That is because the reported rates are not rates of unintended pregnancies in women taking hormonal contraceptives, but the frequencies of reports of unintended pregnancies as a proportion of all reports of suspected adverse reactions. It is the ratios of frequencies that are important. In other words, whatever the baseline risk is, the risk is 13 times higher with enzyme inducers and seven times higher with non-enzyme inducing antibiotics. Because of the possibility of reporting bias the true ratios are probably lower, but unlikely to approach one, in view of the positive control results.
We included a group of enzyme-inducing drugs as a positive control, because it is known that there is an increased risk of an unintended pregnancy if a woman taking a hormonal contraceptive also takes an enzyme-inducing drug. Thus, the Yellow Card data confirm the signal; this shows that analysis of the database is capable of revealing a known interaction. We also included fetal malformations as an outcome, since some of the enzyme-inducing drugs are known to be teratogenic. Again, the database revealed the known signal, even though not all of the enzyme inducers have been associated with teratogenicity, and the size of the signal associated with those that have is therefore probably greater than the data suggest. Further support for the usefulness of the database comes from the inclusion of negative control outcomes (cardiac arrhythmias and headache), which would not be expected to yield a signal, and which did not.
“Pharmacologically, the progestin component of combined oral contraceptives provides the main contraceptive effect” The estrogenic component in a formulation also contributes to inhibition of ovulation, by an action on FSH. This point in fact strengthens the observation that this interaction is likely to be experienced by only a subset of women, those in whom a perturbation of the amount of unbound estrogen to which they are exposed is enough to make a difference between effective and ineffective contraception.
“it is important to not create false concern” We believe that it is more important that women should not be advised that the interaction does not exist, thus potentially exposing them to the risk of an unintended pregnancy. Women should be informed about the possibility of an interaction and be empowered to decide for themselves what to do about their contraceptive practices during short courses of antibiotics. During longer courses of antibiotics (more than 3–6 weeks), it is likely that the intestinal bacteria become resistant to the effects of commonly used antibiotics [1] and that the risk of an unintended pregnancy is much less, assuming that the mechanism is mediated by an effect on gut bacteria. However, we have no data to support advice in such cases, and that is a question that could be usefully researched.
We expect that others will find reasons for denying the existence of this interaction. However, UK Summaries of Product Characteristics (“labels”) continue to warn about it [2,3,4] and even those who have not found confirmatory evidence in formal studies have acknowledged, for example, that women “should be advised that this antibiotic/OC controversy exists” [5].
References
1. Zlitni, Bishara A, Moss EL, Tkachenko E, Kang JB, Culver RN, Andermann TM, Weng Z, Wood C, Handy C, Ji HP, Batzoglou S, Bhatt AS. Strain-resolved microbiome sequencing reveals mobile elements that drive bacterial competition on a clinical timescale. Genome Med 2020; 12: 50.
2. Flamingo Pharma. Amoxicillin 500 mg capsules. https://www.medicines.org.uk/emc/product/11312/smpc.
3. Intrapharma Laboratories Ltd. Oxytetracycline 250 mg tablets. https://www.medicines.org.uk/emc/product/ 4175/smpc.
4. Aspen. Co-trimoxazole 80/400 mg tablets. https://www.medicines.org.uk/emc/product/ 6999/smpc.
5. Helms SE, Bredle DL, Zajic J, Jarjoura D, Brodell RT, Krishnarao I. Oral contraceptive failure and oral antibiotics. J Am Acad Dermatol 1997; 36(5 Pt 1): 705-10.
We read with great interest the recent publication by Prager et al in BMJ Evidence-Based Medicine (1) and commend the authors on their important work. The authors characterize blinding practices in point-of-care ultrasound (POCUS) diagnostic accuracy clinical research. The authors evaluated whether the interpreter was blinded to patient clinical information in articles published in Emergency Medicine, Anesthesia, and Critical Care journals from January 2016 to 2020. Among 97 studies, the authors found that the POCUS interpreter was blinded to clinical information in 38.1% of studies, not blinded in 35.1%, and that the blinding practice was not reported in 26.8%. They additionally report that the same person obtained and interpreted images in 74.2% of studies, was different in 14.4%, and was not reported in 11.3%. These results demonstrate significant variability in POCUS research, leading the authors to conclude that to ensure generalizability of future research, the same person should perform and interpret the POCUS scan and not be blinded to clinical information.
The authors are firm in their recommendation and its perceived benefit. We believe, however, that it is short-sighted to uniformly recommend a study design in this rapidly evolving field. The authors (and importantly, future researchers) should carefully weigh the advantages and disadvantages of differing study designs. Both blinding and not blinding to clinical information allow co...
We read with great interest the recent publication by Prager et al in BMJ Evidence-Based Medicine (1) and commend the authors on their important work. The authors characterize blinding practices in point-of-care ultrasound (POCUS) diagnostic accuracy clinical research. The authors evaluated whether the interpreter was blinded to patient clinical information in articles published in Emergency Medicine, Anesthesia, and Critical Care journals from January 2016 to 2020. Among 97 studies, the authors found that the POCUS interpreter was blinded to clinical information in 38.1% of studies, not blinded in 35.1%, and that the blinding practice was not reported in 26.8%. They additionally report that the same person obtained and interpreted images in 74.2% of studies, was different in 14.4%, and was not reported in 11.3%. These results demonstrate significant variability in POCUS research, leading the authors to conclude that to ensure generalizability of future research, the same person should perform and interpret the POCUS scan and not be blinded to clinical information.
The authors are firm in their recommendation and its perceived benefit. We believe, however, that it is short-sighted to uniformly recommend a study design in this rapidly evolving field. The authors (and importantly, future researchers) should carefully weigh the advantages and disadvantages of differing study designs. Both blinding and not blinding to clinical information allow comprehensive evaluation of POCUS for educational uses, quality improvement, and accurate integration into clinical care. The translational science research spectrum provides a framework, from proof of concept to population level outcomes research (2), among which POCUS research undoubtedly falls. Bias, validity, reliability, reproducibility, and the research question are all important considerations researchers need to consider in developing their study design (3, 4).
We disagree with the author’s assertion that research biases are an intrinsic limitation to POCUS research methodology. Importantly, these biases should not be disregarded by unifying research methodology. As an example, researchers evaluating unstudied POCUS techniques will require a different study design than research evaluating a well-established technique, due to differing research questions; even if the final research outcome is the same.
While Prager et al have highlighted differences in study design and limitations to the performance of meta-analyzes because of significant heterogeneity, we would highly encourage prospective researchers to carefully determine the purpose of their project and to design studies to best answer their question while maximizing scientific rigor. We agree with the author’s that applicability of POCUS research to a generalized clinical setting is optimized by tailoring the study design to real-world application but this is not the sole purpose of ultrasound research which also includes education, monitoring, and quality improvement. Each researcher needs to consider his or her study purpose, and design a study to meet that purpose.
References:
1. Prager R, Wu K, Bachar R, et al. Blinding practices during acute point-of-care ultrasound research: the BLIND-US meta-research study. BMJ Evid Based Med. 2020 Nov 11: bmjebm-2020-111577. doi: 10.1136/bmjebm-2020-111577. Epub ahead of print. PMID: 33177166.
2. Westfall JM, Mold J, Fagnan L. Practice-Based Research— “Blue Highways” on the NIH Roadmap. JAMA. 2007; 297(4): 403–406. doi:10.1001/jama.297.4.403.
3. Stone JC, Glass K, Clark J, et al. A unified framework for bias assessment in clinical research. Int J Evid Based Healthc. 2019 Jun;17(2):106-120. doi: 10.1097/XEB.0000000000000165. PMID: 31094882.
4. Simundić AM. Bias in research. Biochem Med (Zagreb). 2013; 23(1):12-5. doi: 10.11613/bm.2013.003. PMID: 23457761; PMCID: PMC3900086.
The Editor
Read with interest the article
" Effectiveness of honey for symptomatic relief in upper respiratory tract infections: a systematic review and meta-analysis"
Symptomatic relief and treatment of infections are entirely different treatment goals.
A clinician must decide very clearly either on clinical grounds or with investigations, if the infection is going to be a selflimited one which will subside completely without any antimicrobial and also will not cause any late Sequelae. A very important example in this regards used to be Streptococcal throat infections which often would subside without proper antimicrobial treatment, only to cause Rheumatic Fever, Rheumatic Arthritis and Rheumatic Heart Disease later. Not necessarily upper respiratory tract infections, post Streptococcal Glomerulonephritis, post Rickettsial complications are some of the examples where not symptomatic relief, but prompt and adequuate treatment of infections with antimicrobials is crucial for preventing devastating Sequelae.
It is often very difficult to to foresee which respiratory or for that matter any infection will be self limited and will not cause any serious Sequelae if no antimicrobials are used.
That is the CATCH!
Arvind Joshi;
MBBS, MD; FCGP, FAMS;
Founder Convener and President:
Our Own Discussion Group,
602-C, Megh Apartments,
Ganesh Peth Lane, Dadar West;
Mumbai PIN 400028;
Consaltant...
The Editor
Read with interest the article
" Effectiveness of honey for symptomatic relief in upper respiratory tract infections: a systematic review and meta-analysis"
Symptomatic relief and treatment of infections are entirely different treatment goals.
A clinician must decide very clearly either on clinical grounds or with investigations, if the infection is going to be a selflimited one which will subside completely without any antimicrobial and also will not cause any late Sequelae. A very important example in this regards used to be Streptococcal throat infections which often would subside without proper antimicrobial treatment, only to cause Rheumatic Fever, Rheumatic Arthritis and Rheumatic Heart Disease later. Not necessarily upper respiratory tract infections, post Streptococcal Glomerulonephritis, post Rickettsial complications are some of the examples where not symptomatic relief, but prompt and adequuate treatment of infections with antimicrobials is crucial for preventing devastating Sequelae.
It is often very difficult to to foresee which respiratory or for that matter any infection will be self limited and will not cause any serious Sequelae if no antimicrobials are used.
That is the CATCH!
Arvind Joshi;
MBBS, MD; FCGP, FAMS;
Founder Convener and President:
Our Own Discussion Group,
602-C, Megh Apartments,
Ganesh Peth Lane, Dadar West;
Mumbai PIN 400028;
Consaltant Physician at Ruchi Diagnostic Center and Ruchi Clinical Laboratory, Sunshine CHS, Plot 58,
Kharghar PIN 410210,
Maharashtra State, INDIA.
FICP
It is risky to propose that agent offering symptomatic relief should replace microbial cure. Two are different aspects and different approaches.
Besides honey may not be considered entirely safe. Many environmental Journals are raising voice against contamination of honey either by microbes or by antimicrobials.
Clinicians must know if the Upper Respiratory Infection is going to be entirely selflimited and will not progress to Pneumonia, or lead to late Sequelae like Rheumatic Fever Rheumatic Heart Disease.
If only symptomatic relief is to be achieved, one wonders if home made sugar syrup may work as well as honey will. Moreover homemade sugar syrup will not carry microbes or antimicrobials!
Arvind Joshi MBBS MD FCGP FAMS FICP.
I read with interest the latest evidence for honey and treatment of coughs which was also reported widely in the national press (1). Honey has been shown in laboratory in vitro studies to inhibit bacterial growth including Helicobacter pylori linked with dyspepsia and gastritis (2, 3). Concentrations between 10-20% honey has been shown to be effective against both Gram negative and Gram positive bacteria (3). My late father Professor MNH Chowdhury, a clinical bacteriologist, researched this in the 1990s and advocated Manuka honey especially for its healing and antibacterIal properties. Interestingly, the in vitro findings showed some isolates were resistant to various antimicrobial agents but honey inhibited these organisms also (3). Secondary bacterial infections may respond to this simple remedy after primary viral coughs and colds and need further clinical study.
References
1. Abuelgasim H, Albury C, Lee J. Effectiveness of honey for symptomatic relief in upper respiratory tract infections: a systematic review and meta-analysis. BMJ Evidence Based Med 2020, 18 Aug online; bmjebm-2020-111336.
2. Rashed RS, Ayoola EA, Mofleh IA, Chowdhury MNH, Mahmood K, Faleh FZ. Helicobacter pylori and dyspepsia in an Arab population. Trop Geogr Med 1992; 44(4), 304-7.
3. Ali AT, Chowdhury MNH, al Humayyad MS. Inhibitory effect of natural honey on Helicobacter pylori. Trop Gastroenterol 1991; 12(3), 139-43.
We read the article “Effectiveness of honey for symptomatic relief in upper respiratory tract infections: a systematic review and meta-analysis” with great interest. The need to discover effective remedies for symptomatic relief of upper respiratory tract infections (URTIs), while preventing further antimicrobial resistance developing is indeed paramount. However, after reading the article in detail, we noted a number of discrepancies which we feel must be highlighted and addressed.
Firstly, we believe that the article is misleading, and if read as a lay member of the public, or indeed by a sensationalist news outlet, incorrect and potentially health-threatening conclusions may be drawn and promoted. Firstly, the abstract focuses on positing honey as an alternative to antibiotics for the symptomatic relief of URTIs. The authors highlight that honey possesses antimicrobial properties, with the conclusion of the abstract affirming that it is a “widely available and cheap alternative to antibiotics”. The abstract also concludes that honey improves symptoms in comparison with “usual care”, which, left hitherto unspecified, and paired with the aforementioned focus on a comparison between honey and antibiotics, again augments the misleading introduction to the article. Fundamentally, none of the 14 the studies included within the systematic review compare the use of honey with the use of antibiotics. Focusing so strongly on comparing honey to antib...
We read the article “Effectiveness of honey for symptomatic relief in upper respiratory tract infections: a systematic review and meta-analysis” with great interest. The need to discover effective remedies for symptomatic relief of upper respiratory tract infections (URTIs), while preventing further antimicrobial resistance developing is indeed paramount. However, after reading the article in detail, we noted a number of discrepancies which we feel must be highlighted and addressed.
Firstly, we believe that the article is misleading, and if read as a lay member of the public, or indeed by a sensationalist news outlet, incorrect and potentially health-threatening conclusions may be drawn and promoted. Firstly, the abstract focuses on positing honey as an alternative to antibiotics for the symptomatic relief of URTIs. The authors highlight that honey possesses antimicrobial properties, with the conclusion of the abstract affirming that it is a “widely available and cheap alternative to antibiotics”. The abstract also concludes that honey improves symptoms in comparison with “usual care”, which, left hitherto unspecified, and paired with the aforementioned focus on a comparison between honey and antibiotics, again augments the misleading introduction to the article. Fundamentally, none of the 14 the studies included within the systematic review compare the use of honey with the use of antibiotics. Focusing so strongly on comparing honey to antibiotics, both within the abstract and throughout the article, with the conclusion stating that authors “would recommend honey as an alternative to antibiotics”, is unjustified, and may have potentially dangerous implications for those misled by the statements.
The statements regarding antibiotics themselves are also both vague and misleading. Authors state that “the use of antibiotics for URTIs is a particular problem, because they are ineffective”, which, as a sweeping statement, is highly inaccurate. The claim that antibiotics are “associated with significant adverse effects in children and adults” is also imprecise and over-generalised, again contributing to the article’s potential to both misinform readers and promote scaremongering. We also feel there should also be more clarity with regards to the age restrictions surrounding the therapeutic recommendations for honey. While the authors briefly mention within their discussion that honey is not commercially safe for those who are allergic and infants under 1 years old, there is no mention of any age limitations within the introduction and conclusion section of this statement being made.
It must be noted that the studies included within the systematic review contain high levels of bias, which limits both the reliability of the results and the conclusions made. For instance, authors utilise the Cochrane risk of bias tool, which states that the overall risk of bias for each article is the lowest favourable assessment of all domains [1]. Therefore, according to Figure 2 of the article, a “Summary of risk of bias assessment for included studies” - for which no key is provided - 9 of the studies are classified as having a ‘high risk’ of bias, with 5 classified as having ‘some concerns’. This is contrary to what is stated in the article; authors claim that two articles were at ‘low risk’ of bias, with the overall risk of bias being ‘moderate’. Authors therefore seem to have assigned a lower level of bias to the studies than classified by the Cochrane risk of bias tool, which, paired with the fact that the majority of the studies included have a high risk of bias, further acts to decrease the reliability of the conclusions made. Additionally, the high level of disparity between the variables within the studies decreases the validity of the conclusions even further. There are over 14 variations of interventions, and 10 variations of comparators, between the 14 studies. This high level of bias and variability amongst the studies included thus renders the findings of the systematic review, and therefore the ability to
judge the efficacy of honey on URTIs, highly limited.
Furthermore, it is important to maintain appropriate antimicrobial stewardship when practicing medicine. However, this article provides little delineation as to what particular organisms honey would be effective against. For instance, not all members of the public will be aware that antibiotics are ineffective against viral infections. Whilst the authors state “the majority of URTI’s are viral, therefore antibiotics would be ineffective” – there is little mention with regards to bacterial, fungal or helminthic organisms – and the vagueness of the statement above could be considered misleading. Having shown this article to persons of a non-medical background, it became obvious that there was a lack of clarity, creating confusion as to whether honey should be used for all organisms, or just viral ones. Additionally, the National Institute of Clinical Excellence (NICE) recommends Phenoxymethylpenicillin or Clarithromycin/Erythromycin for the treatment of patients with suspected bacterial URTIs, who score high enough using the FeverPAIN or Centor score [2]. Readers of this paper may wrongly be given the impression that honey supersedes the use of antibiotics for any infection, and therefore treat themselves or others in their care as such. With some infections, such as streptococcus, having the potential to cause significant morbidity if left untreated by antibiotics [3], the misinformation within this article could lead to the development of rheumatic fever and cardiac complications later in life.
Ultimately, our aforementioned points; the lack of clarity throughout the article, the bias within each study, and the significant variability between the studies’ variables combine to create a misleading article, with potentially damaging consequences for the lay public. Dangerous decisions could ultimately be made, with our main concern being that people may delay seeking appropriate medical help for a condition for which honey is ultimately not the appropriate treatment; in turn this could increase both morbidity and use of NHS resources. With the propensity for news outlets to grasp for controversial headlines, and promoting them in a further misleading and sensationalist manner, we feel that a more balanced argument needs to be put forward, in order for a responsible message on this interesting, pertinent topic to be conveyed.
1. Chapter 8: Assessing risk of bias in a randomized trial | Cochrane Training. https://training.cochrane.org/handbook/current/chapter-08. Accessed October 2, 2020.
2. Respiratory Tract Infections-Antibiotic Prescribing Prescribing of Antibiotics for Self-Limiting Respiratory Tract Infections in Adults and Children in Primary Care. www.nice.org.uk. Accessed October 2, 2020.
3. Thompson KM, Sterkel AK, McBride JA, Corliss RF. The Shock of Strep: Rapid Deaths Due to Group a Streptococcus. Acad Forensic Pathol. 2018. doi:10.23907/2018.010
It would be helpful if it assessed the standard administration quantitatively and specific frequency utilized in the study ‘s participants , or related studies , At the very least - providing a link to the exact dosing used in this study as a reference point would be beneficial .
Thank you for this measured summary of the recently published HYGIA trial. I am pleased to see you mention the BedMed study ongoing. Readers may be interested to know that there is another study, already in follow-up, which will provide further evidence on whether night-time dosing of blood pressure medications really is better in the prevention of cardiovascular events and mortality.
The University of Dundee's Treatment in Morning vs Evening (TIME, www.timestudy.co.uk) study, funded by the British Heart Foundation, aims to answer the same research question. TIME has recruited 21,104 participants across the UK and should finish in the first half of 2020.
Like so many purported pundits, DuBroff R, de Lorgeril M [1] have attempted to dispute the significance of the role of saturated fat (triglycerides) and LDL-cholesterol in the development of coronary artery disease, while noting the importance of inflammation itself [1,2]. In law, ignorance of the law is not a defense - the same is true for medicine. Not understanding something does not make you an expert [2] and it does not make your argument valid. Appealing to the court of public opinion does not make it so either. Accordingly, we present a brief explanation of why the authors [1,2] – and others – have presented an invalid discussion of the role fat and LDL-cholesterol plays in coronary artery disease.
In the mid-1990s, as one of the reviewers for the American Heart Association, the first author of this letter, Dr Richard M Fleming (RMF) introduced a then controversial theory stating that Coronary Artery Disease (CAD) is the result of an inflammatory process, which builds up within the walls of the arteries impairing their ability to dilate and increase coronary blood flow when needed; thus producing regional blood flow differences resulting in angina [3-6] and ultimately myocardial infarction (MI) and death.
In recent years, people promoting various dietary and lifestyle practices – particularly those promoting LowCarb-Keto diets, have used the obesity epidemic to focus attention on obesity and weight loss. These same individuals have not demonstrated th...
Like so many purported pundits, DuBroff R, de Lorgeril M [1] have attempted to dispute the significance of the role of saturated fat (triglycerides) and LDL-cholesterol in the development of coronary artery disease, while noting the importance of inflammation itself [1,2]. In law, ignorance of the law is not a defense - the same is true for medicine. Not understanding something does not make you an expert [2] and it does not make your argument valid. Appealing to the court of public opinion does not make it so either. Accordingly, we present a brief explanation of why the authors [1,2] – and others – have presented an invalid discussion of the role fat and LDL-cholesterol plays in coronary artery disease.
In the mid-1990s, as one of the reviewers for the American Heart Association, the first author of this letter, Dr Richard M Fleming (RMF) introduced a then controversial theory stating that Coronary Artery Disease (CAD) is the result of an inflammatory process, which builds up within the walls of the arteries impairing their ability to dilate and increase coronary blood flow when needed; thus producing regional blood flow differences resulting in angina [3-6] and ultimately myocardial infarction (MI) and death.
In recent years, people promoting various dietary and lifestyle practices – particularly those promoting LowCarb-Keto diets, have used the obesity epidemic to focus attention on obesity and weight loss. These same individuals have not demonstrated the actual impact their diets have on CAD, anymore than BigPharma has by reporting changes in lipid levels using their drugs. To demonstrate such change in CAD - either by drug or dietary intervention - requires more than the mere showing of changes in weight or serum blood tests as discussed infra. It requires the actual measurement of the changes occurring within the walls of the coronary arteries themselves – not some other artery – where the actual inflammation and resulting change in coronary artery function exists [3,6].
The arguments presented by DuBroff [1] and Ravnskov [2] erroneously use studies measuring lipid and inflammatory surrogate markers - blood tests - to support their position, while others [7] use this same approach to support their dietary recommendations by showing weight loss, and occasionally reductions in cholesterol levels – at least initially in some people. As more studies have been done, it has been shown that these initial reductions in lipid levels either do not occur for everyone or are followed by a subsequent increase. This has forced the purported diet pundits to support the position that LDL-cholesterol and saturated (triglycerides) fat do not clog the (coronary or other) arteries [7].
For the authors [1,2,7] to declare that saturated fat and LDL-cholesterol have nothing to do with the development of inflammatory CAD demonstrates a complete failure to understand the “Inflammation and Heart Disease” Theory [5,8], or a failure to have read it, and therefore cannot be taken seriously.
The specific claims made by Malhotra [7] introduces yet another major misconception into the discussion of CAD. Specifically, the process of “clogging of the coronary arteries.” The narrowing or “clogging” of the coronary artery lumen – where the blood flows - so frequently referred to as CAD, is actually a late process in the development of the inflammatory changes that are CAD [9-15].
CAD begins with an inflammatory process, which first distends the wall of the artery outward away from the lumen – impairing the function of the artery - and only later encroaches upon the coronary lumen itself [3,5,9]. Recognition that the rupture of this inflammatory process may occur following minimal or no coronary lumen narrowing [3-5,9] has resulted in the recent acknowledgement by the Cardiology community that infarction of myocardium may occur with (Type I) or without (TYPE II) coronary lumen obstruction.
Fleming and Harrington’s research published in 2008 [16] demonstrated that the relationship between weight loss, and changes in lipids and other blood tests reflecting inflammatory processes [5], are only mildly-to-moderately correlated with actual changes occurring within the coronary arteries themselves. Thus further exposing the erroneous artery “clogging” statement - using the results of blood tests – to declare that saturated fat and cholesterol are not involved in CAD.
To understand the impact LowCarb-Keto diets - or for that matter any diet or drug treatment - has on CAD, one needs to measure what is actually happening to the coronary arteries themselves [17-19]; quantitatively now made possible using FMTVDM [6].
To state that Saturated fat and LDL-cholesterol has nothing to do with CAD and do not result in the “clogging” of coronary arteries or CAD itself, and then to state that CAD is a chronic inflammatory condition - raises serious concerns about the motivation and integrity of their arguments. It also raises serious questions about their actual understanding of the ”Inflammation and Heart Disease” and “Angina” Theories [3,5,20]. Ignorance is not bliss - “we can teach it to you, but we cannot understand it for you.”
We are sadly reminded of these words from Billy Madison:
“Mr. Madison, what you just said is one of the most insanely idiotic things I have ever heard. At no point in your rambling incoherent response were you even close to anything that could be considered a rational thought. Everyone in this room is now dumber for having listened to it. I award you no points and may God have mercy on your soul.”
Acknowledged potential COI: FMTVDM (The Fleming Method for Tissue and Vascular Differentiation and Metabolism) [6] is issued to the first author. The first author authored the “Inflammation and Heart Disease” and “Angina” Theories.
References:
1. DuBroff R, de Lorgeril M. Fat or fiction: the diet-heart hypothesis. BMJ Evidence-Based Medicine 2019 doi:10.1136/bmjebm-2019-111180.
2. Ravnskov U, de Lorgeril M, Diamond DM, et al. LDL-C does not cause cardiovascular disease: a comprehensive review off the current literature. Expert review of clinical pharmacology
3. Fleming RM. Chapter 29. Atherosclerosis: Understanding the relationship between coronary artery disease and stenosis flow reserve. Textbook of Angiology. John C. Chang Editor, Springer-Verlag, New York, NY. 1999. pp. 381-387.
4. Fleming RM. Chapter 30. Cholesterol, Triglycerides and the treatment of hyperlipidemias. Textbook of Angiology. John C. Chang Editor, Springer-Verlag, New York, NY. 1999, pp. 388-396.
5. Fleming RM. Chapter 64. The Pathogenesis of Vascular Disease. Textbook of Angiology. John C. Chang Editor, Springer-Verlag New York, NY. 1999, pp. 787-798.
6. The Fleming Method for Tissue and Vascular Differentiation and Metabolism (FMTVDM) using same state single or sequential quantification comparisons. Patent Number 9566037. Issued 02/14/2017.
7. Malhotra A, Redberg R, Meier P. Saturated fat does not clog the arteries: coronary heart disease is a chronic inflammatory condition, the risk of which can be effectively reduced from healthy lifestyle interventions. British J Sports Med 2017;51:1111-1112.
8. 20/20 Segment on Heart Disease and Inflammation. https://www.youtube.com/watch?v=Hvb_Ced7KyA&t=22s
9. Glagov S, Weisenberg E, Zarins CK, Stankunavicius R, Kolettis GJ. Compensatory enlargement of human atherosclerotic coronary arteries. N Engl J Med 1987;316(22):1371-1375.
10. Fleming RM., Kirkeeide RL, Smalling RW, Gould KL. Patterns in Visual Interpretation of Coronary Arteriograms as Detected by Quantitative Coronary Arteriography. J Am Coll. Cardiol. 1991;18:945- 951.
11. Fleming RM, Harrington GM. Quantitative Coronary Arteriography and its Assessment of Atherosclerosis. Part 1. Examining the Independent Variables. Angiology 1994;45(10):829-833.
12. Fleming RM, Harrington GM. Quantitative Coronary Arteriography and its Assessment of Atherosclerosis. Part 2. Calculating Stenosis Flow Reserve Directly from Percent Diameter Stenosis. Angiology 1994;45(10):835-840.
13. Fleming RM. Shortcomings of coronary angiography. Letter to the Editor. Cleve Clin J Med 2000;67:450.
14. Fleming RM. Coronary Artery Disease is More than Just Coronary Lumen Disease. Amer J Card 2001;88:599-600.
15. Fleming RM, Harrington GM. TAM-A.7 Sestamibi redistribution measurement defines ischemic coronary artery lumen disease. 56th Annual Meeting of the Health Physics Society. (American Conference of Radiological Safety) West Palm Beach, FL, USA, 30 June 2011. http://hpschapters.org/2011AM/program/singlesession.php3?sessid=TAM-A
16. Fleming RM, Harrington GM. What is the Relationship between Myocardial Perfusion Imaging and Coronary Artery Disease Risk Factors and Markers of Inflammation? Angiology 2008;59:16-25.
17. Fleming RM, Fleming MR, Chaudhuri TK. Replacing Cardiovascular Risk Factors with True AI and Absolute Quantifiable Measurement (FMTVDM) of Coronary Artery Disease. Inter J Res Studies Med & Health Sci. 2019;4(11):11- 13. ISSN:2456-6373.
18. Fleming RM, Fleming MR, Chaudhuri TK. Are we prescribing the right diets and drugs for CAD, T2D, Cancer and Obesity? Int J Nuclear Med Radioactive Subs 2019;2(2):000115.
19. Fleming RM, Fleming MR, Chaudhuri TK, Harrington GM. Cardiovascular Outcomes of Diet Counseling. Edel J Biomed Res Rev. 2019;1(1):20-29.
20. Fleming RM., Boyd L., Forster M. Angina is Caused by Regional Blood Flow Differences - Proof of a Physiologic (Not Anatomic) Narrowing, Joint Session of the European Society of Cardiology and the American College of Cardiology, Annual American College of Cardiology Scientific Sessions, Anaheim, California, USA, 12 March 2000, 49th (Placed on internet www.prous.com for physician training and CME credit, April 2000.)
The Murphy et al. letter1 is notable for its ad hominem claims, the first of which comes in their introductory remarks. Noting that my review2 reports no conflicts of interest, they make the exaggerated claim that I have “written extensively on the ‘lethality’ of caffeine”. That claim cites one published article, titled “Death by Caffeine”,3 which summarises reports of death by poisoning involving documented cases from coronial and other official public inquiries. As reported in that article, official records in several countries report multiple confirmed cases of death by poisoning due to caffeine. Although relatively rare, such cases have been (and continue to be) reported worldwide. Predicated on the mere fact that I have previously reported findings from official inquiries into caffeine-related harm, the claim by Murphy et al. of “conflict” is perverse. By implication, their reasoning would mean that the reporting of harm from any source (which includes much of the content of medical journals) renders authors (i.e., most medical researchers) evermore vulnerable to bias warranting formal disclosure of conflict of interest in all future reports on the same or related topic. Of course, no such custom or practice exists.
Notably, the assertion of conflict in this instance indicates poor understanding of the matter, a lamentable situation considering the professional identities of Murphy and her 20 co-authors. Conflict of interest arises when a primary interest conf...
Show MoreDrs Clure and Lazorwitz have misunderstood and misinterpreted the Yellow Card data that we adduced to test the null hypothesis that there is no interaction of antibiotics with hormonal contraceptives. Here we reply to their specific comments.
“The medications in each group are not equivalent and bias the sample” We chose a wide range of medicines in order to minimize this. Clure and Lazorwitz have selected only two examples each from the group of nine control drugs and the group of nine non-enzyme-inducing antibiotics, and assert that the age distribution favours older women in the control group. However, they ignore the fact that the same could be asserted of the enzyme-inducing drugs, some of which are more likely to be used in older women, but had an even bigger effect than the antibiotics.
“The rates of unintended pregnancy reported … are much lower than expected in general users of oral contraception” This is an important misunderstanding, which we sought to obviate in the paper, by making it clear that the data do not allow calculation of the absolute rates of unintended pregnancies. That is because the reported rates are not rates of unintended pregnancies in women taking hormonal contraceptives, but the frequencies of reports of unintended pregnancies as a proportion of all reports of suspected adverse reactions. It is the ratios of frequencies that are important. In other words, whatever the baseline risk is, the risk is 13 times higher with enzyme i...
Show MoreTo the Editor,
We read with great interest the recent publication by Prager et al in BMJ Evidence-Based Medicine (1) and commend the authors on their important work. The authors characterize blinding practices in point-of-care ultrasound (POCUS) diagnostic accuracy clinical research. The authors evaluated whether the interpreter was blinded to patient clinical information in articles published in Emergency Medicine, Anesthesia, and Critical Care journals from January 2016 to 2020. Among 97 studies, the authors found that the POCUS interpreter was blinded to clinical information in 38.1% of studies, not blinded in 35.1%, and that the blinding practice was not reported in 26.8%. They additionally report that the same person obtained and interpreted images in 74.2% of studies, was different in 14.4%, and was not reported in 11.3%. These results demonstrate significant variability in POCUS research, leading the authors to conclude that to ensure generalizability of future research, the same person should perform and interpret the POCUS scan and not be blinded to clinical information.
The authors are firm in their recommendation and its perceived benefit. We believe, however, that it is short-sighted to uniformly recommend a study design in this rapidly evolving field. The authors (and importantly, future researchers) should carefully weigh the advantages and disadvantages of differing study designs. Both blinding and not blinding to clinical information allow co...
Show MoreThe Editor
Show MoreRead with interest the article
" Effectiveness of honey for symptomatic relief in upper respiratory tract infections: a systematic review and meta-analysis"
Symptomatic relief and treatment of infections are entirely different treatment goals.
A clinician must decide very clearly either on clinical grounds or with investigations, if the infection is going to be a selflimited one which will subside completely without any antimicrobial and also will not cause any late Sequelae. A very important example in this regards used to be Streptococcal throat infections which often would subside without proper antimicrobial treatment, only to cause Rheumatic Fever, Rheumatic Arthritis and Rheumatic Heart Disease later. Not necessarily upper respiratory tract infections, post Streptococcal Glomerulonephritis, post Rickettsial complications are some of the examples where not symptomatic relief, but prompt and adequuate treatment of infections with antimicrobials is crucial for preventing devastating Sequelae.
It is often very difficult to to foresee which respiratory or for that matter any infection will be self limited and will not cause any serious Sequelae if no antimicrobials are used.
That is the CATCH!
Arvind Joshi;
MBBS, MD; FCGP, FAMS;
Founder Convener and President:
Our Own Discussion Group,
602-C, Megh Apartments,
Ganesh Peth Lane, Dadar West;
Mumbai PIN 400028;
Consaltant...
It is risky to propose that agent offering symptomatic relief should replace microbial cure. Two are different aspects and different approaches.
Besides honey may not be considered entirely safe. Many environmental Journals are raising voice against contamination of honey either by microbes or by antimicrobials.
Clinicians must know if the Upper Respiratory Infection is going to be entirely selflimited and will not progress to Pneumonia, or lead to late Sequelae like Rheumatic Fever Rheumatic Heart Disease.
If only symptomatic relief is to be achieved, one wonders if home made sugar syrup may work as well as honey will. Moreover homemade sugar syrup will not carry microbes or antimicrobials!
Arvind Joshi MBBS MD FCGP FAMS FICP.
I read with interest the latest evidence for honey and treatment of coughs which was also reported widely in the national press (1). Honey has been shown in laboratory in vitro studies to inhibit bacterial growth including Helicobacter pylori linked with dyspepsia and gastritis (2, 3). Concentrations between 10-20% honey has been shown to be effective against both Gram negative and Gram positive bacteria (3). My late father Professor MNH Chowdhury, a clinical bacteriologist, researched this in the 1990s and advocated Manuka honey especially for its healing and antibacterIal properties. Interestingly, the in vitro findings showed some isolates were resistant to various antimicrobial agents but honey inhibited these organisms also (3). Secondary bacterial infections may respond to this simple remedy after primary viral coughs and colds and need further clinical study.
References
1. Abuelgasim H, Albury C, Lee J. Effectiveness of honey for symptomatic relief in upper respiratory tract infections: a systematic review and meta-analysis. BMJ Evidence Based Med 2020, 18 Aug online; bmjebm-2020-111336.
2. Rashed RS, Ayoola EA, Mofleh IA, Chowdhury MNH, Mahmood K, Faleh FZ. Helicobacter pylori and dyspepsia in an Arab population. Trop Geogr Med 1992; 44(4), 304-7.
3. Ali AT, Chowdhury MNH, al Humayyad MS. Inhibitory effect of natural honey on Helicobacter pylori. Trop Gastroenterol 1991; 12(3), 139-43.
To the editor,
We read the article “Effectiveness of honey for symptomatic relief in upper respiratory tract infections: a systematic review and meta-analysis” with great interest. The need to discover effective remedies for symptomatic relief of upper respiratory tract infections (URTIs), while preventing further antimicrobial resistance developing is indeed paramount. However, after reading the article in detail, we noted a number of discrepancies which we feel must be highlighted and addressed.
Firstly, we believe that the article is misleading, and if read as a lay member of the public, or indeed by a sensationalist news outlet, incorrect and potentially health-threatening conclusions may be drawn and promoted. Firstly, the abstract focuses on positing honey as an alternative to antibiotics for the symptomatic relief of URTIs. The authors highlight that honey possesses antimicrobial properties, with the conclusion of the abstract affirming that it is a “widely available and cheap alternative to antibiotics”. The abstract also concludes that honey improves symptoms in comparison with “usual care”, which, left hitherto unspecified, and paired with the aforementioned focus on a comparison between honey and antibiotics, again augments the misleading introduction to the article. Fundamentally, none of the 14 the studies included within the systematic review compare the use of honey with the use of antibiotics. Focusing so strongly on comparing honey to antib...
Show MoreIt would be helpful if it assessed the standard administration quantitatively and specific frequency utilized in the study ‘s participants , or related studies , At the very least - providing a link to the exact dosing used in this study as a reference point would be beneficial .
Thank you for this measured summary of the recently published HYGIA trial. I am pleased to see you mention the BedMed study ongoing. Readers may be interested to know that there is another study, already in follow-up, which will provide further evidence on whether night-time dosing of blood pressure medications really is better in the prevention of cardiovascular events and mortality.
The University of Dundee's Treatment in Morning vs Evening (TIME, www.timestudy.co.uk) study, funded by the British Heart Foundation, aims to answer the same research question. TIME has recruited 21,104 participants across the UK and should finish in the first half of 2020.
Like so many purported pundits, DuBroff R, de Lorgeril M [1] have attempted to dispute the significance of the role of saturated fat (triglycerides) and LDL-cholesterol in the development of coronary artery disease, while noting the importance of inflammation itself [1,2]. In law, ignorance of the law is not a defense - the same is true for medicine. Not understanding something does not make you an expert [2] and it does not make your argument valid. Appealing to the court of public opinion does not make it so either. Accordingly, we present a brief explanation of why the authors [1,2] – and others – have presented an invalid discussion of the role fat and LDL-cholesterol plays in coronary artery disease.
In the mid-1990s, as one of the reviewers for the American Heart Association, the first author of this letter, Dr Richard M Fleming (RMF) introduced a then controversial theory stating that Coronary Artery Disease (CAD) is the result of an inflammatory process, which builds up within the walls of the arteries impairing their ability to dilate and increase coronary blood flow when needed; thus producing regional blood flow differences resulting in angina [3-6] and ultimately myocardial infarction (MI) and death.
In recent years, people promoting various dietary and lifestyle practices – particularly those promoting LowCarb-Keto diets, have used the obesity epidemic to focus attention on obesity and weight loss. These same individuals have not demonstrated th...
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