13 e-Letters

  • Psychometric testing of the Norwegian Diabetes Health Profile (DHP-18) in patients with type 1 diabetes

    As author of the Diabetes Health Profile, I felt that overall the paper provided a generally balanced report of your study, I have however, a number of issues regarding your report.

    First, although resulting in a high alpha coefficient (0.79), it is incorrect to calculate an alpha score for the total number of items when the scale itself is multidimensional (Oranges and apples). In doing so, it can result in an overall low alpha score. In this case it is fortunate that the value was high. Had this been a low score this would have been perceived as a negative result to the less knowledgeable.

    Secondly, with regard to responsiveness to change, a crude method for measuring change in score was used together with a very limited patient sample. Although the limitation of the methodology was discussed to some extent in the discussion, it would have been preferable at least to measure at both pre and post for each of the three scale domains. Minimally Important Difference (MID) values are available for the DHP that would enable the smallest change in score that is clinically significant to be measured.

    Thirdly, in the section ‘Significance of the study’ it would have been more appropriate that the final comment on implementation in clinical practice and studies should have been limited to the ‘Norwegian’ version of the DHP-18. As currently phrased this is rather general and suggests the use of the DHP-18 in clinical studies per se.

    Finally, permi...

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  • Bedside diagnosing T2DM from birth is the first activity in the fight against this growing epidemic.

    T2DM first problem still open is to recognize diabetics so far without proper diagnosis, in order to avoid the series of complications that arise decades before the clinical diabetic symptomatology decades before the clinical diabetic symptomatologyFDA Commissioner Scott Gottlieb, MD, said: "Diabetes affects nearly 30 million Americans. Access to affordable insulin is literally a matter of life and death". Aurobindo would say this is a true and false statement. Why do we all, including FDA, not radically solve the real problem underlying the diabetic growing epidemic? Let's start talking about Pre-Primary and Primary Prevention of T2DM, based on Diabetic and Dislipidemic-Dependent, Inherited Real Risk, bedside diagnosed from birth with a stethoscope, and removed by inexpensive Reconstructing Mitochodrial Quantum Therapy. The till now open problem in the traditional Accademic Medicine is the clinical diagnosis of T2DM from the First of its Five Stages. Well. Recently, a new and original reliable clinical method for diagnosing DM has been added to a flurry of methods that have existed for twenty years. The Corpus Callosum is the part of the brainthat allows communication between its two hemispheres. It is responsible for transmitting neural messages between both the right and left hemispheres. According to Angiobiopathy Theory, microvessel dynamic parallels the related parenchima cell activity. As a consequence,thanks to Quantum Biophysical Semeiotic, physi...

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  • Author's Response

    We would like to thank Anne-Thea McGill and Brown et al for their response to our manuscript “Parental history of type 2 diabetes is associated with lower resting energy expenditure in normoglycemic subjects.” The points raised by the commentaries are well taken. However, as stated in the limitations of our study, we performed a cross-sectional study which did not track weight gain A longitudinal study would be required to gain such specific insights. While predictive models are useful, they are not without limitations and the most accurate determination of weight gain arising from lower resting energy expenditure is best done by a longitudinal study. Lower resting expenditure may not always equate to an energy surplus as energy intake could be lower in subjects with lower REE or physical activity energy expenditure may be higher, thus balancing the total energy expenditure.

  • Is added certain portion on Mediterranean Diet highly necessary?

    It’s appreciated for addressing an interesting area of research about the efficacy of medical nutrition treatment based on the Mediterranean Diet (MedDiet).
    The study was a secondary analysis of the St Carlos GDM Prevention Study, conducted between January and December 2015 in Hospital Clinico San Carlos (Madrid, Spain). The author used MedDiet-MNT in order to observe its effects on mother’s glycemic level and also the prenatal outcome.
    According to this study, there were two groups. Both groups received dietary recommendation to follow MD guideline, the difference was just in intervention group, they added portion for virgin olive oil and nuts. Basically both groups had similar diet recommendation, so further clinical experiment is highly needed to determine the exact effect of adding portion in extra virgin olive oil and nuts on lowering risk of GDM.
    Although this diet had several benefits, the use of adding portion on extra virgin oil and pistachios in the intervention group treatment still becomes a question. In the other study, traditional Mediterranean diet had positive effect on lowering risk of GDM in pregnant women (Izadi, 2016), this outcome also occurred in the study conducted by Perez,Ferre (2014) that MD could reduce risk of GDM. So, if the traditional way has been reported successful in lowering GDM risk, is that really necessary to modify the basic guideline of MedDiet?

    1. Izadi V, Tehrani H, Haghighatdoost F, et.a...

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  • Energy Metabolism, particularly in humans, depends on myriads of food micronutrients - far to complex to quantify

    Humans have proportionately large, complex brains that require large amounts of nutrients- energy and micronutrients. There are a number of little recognised co-adaptations to manage this 'brain drain'. Two very important mechanisms to manage this high localised metabolic rate were to - 1) Use the extremely varied and reactive plant chemicals that were increasingly being consumed in the nomadic hunter-gatherer hominins 2) To increase the buffer stores of nutrients by reactivating mammalian genes for subcutaneous fat stores. 3) increase strong drives to acquire high nutrient food predicated on energy density.
    The nutrient chemicals are often plant defence (secondary) chemicals) of which the anti yeast polyphenol resveratrol is but one of myriads, act as Michael acceptors. These reactions are much less precise that enzymatic reactions. They shuffle-reshuffle electrons and efficiently manage energy, reducing free radical production and energy loss . There are a number of enhanced anti-oxidant, detoxification, and adaptive and general cell repair pathways coordinated by the NRF2/Keap1/antioxidant response element cell protection systems.
    2) As mentioned, the subcutaneaous adipose tissue is a brain nutrient buffer - especially for the intra-uterine and postnatal human brain development. This adipose is not just a fat store but lipids and many other nutrients should be in the stores - those absorbed through the colon after being trafficked there...

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  • The 3500 Kcal Rule is Invalid for Projections of Weight Change

    Nyenwe et al. (1) address an interesting and important topic of the effects or associations of parental diabetes with offspring outcomes. However, the paper contains an important error that renders one of their conclusions markedly incorrect.

    Specifically, having estimated a difference in energy expenditure among offspring of parents with diabetes (which the authors refer to as ‘parental diabetes’) versus offspring of parents without diabetes, the authors project that persons with parental diabetes will, as a result of this difference, steadily gain substantial weight indefinitely. They state:

    “According to the data published by Wishnofsky (2), one pound has a caloric value of 3500 kcal or (1 kg=7700 kcal). We derived the estimated weight gain in kg by dividing the projected energy accrual by 7700. When normalized REE is used for this estimation, subjects with parental diabetes had a daily energy surplus of 125 kcal which would translate to ~6 kg weight gain per year.”

    This type of estimation is commonly referred to as the 3500 kcal rule or 3500 kcal per pound rule.

    This reasoning and calculation is erroneous because it fails to account for the dynamic changes of energy expenditure that occur with weight gain and loss. Wishnofsky himself noted the complexity of estimating energetic equivalents of gaining or losing body weight, specifically addressing the importance of time, nitrogen balance, tissue type, and water loss, among other factors, on...

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  • Estrogens and other uncovered associations with diabetes and cardiovascular diseases among female workers

    To the Editor

    We read with great interest the article by Gilbert-Ouimet M et al1 recently published in your journal. Such study showed an interesting result that only increased risk of incidence of diabetes occurring among female workers working 45 hours or more per week, and suggested that modification of such risk factors would be helpful to improve prevention strategies and orient policymaking by following up 7065 workers over a 12-year period in Ontario, Canada.
    However, we have some concerns. Firstly, in order to find out the potential relationship between long work hours and the incidence of diabetes, several other independent variables were considered in the analysis process such as sociodemographic and health-related covariates, but the information of menopause and menopausal hormone therapy (MHT) among women was not added. Strong association with increased risk of cardiovascular diseases had been confirmed in several studies and data from large randomized-controlled trials have shown that the decrease of incidence of T2D in women could be achieved by MHT with conjugated estrogens 2,3 . Although the clinical evidence still not be sufficient to recommend the use of hormones for prevention of diabetes among women especially with early menopause or premature ovarian insufficiency4, such detail might be helpful to uncover the neglected association between menopause and increased risk of diabetes.
    Secondly, compared with the increased risk...

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  • The hot environment hypothesis in diabetes pathophysiology

    Dear editor,

    The study published in a recent volume of the journal by Blauw et al. is an excellent opportunity to highlight an under-examined environmental hypothesis in the pathophysiology of type 2 diabetes.1 In their epidemiological study, the authors used meta-regression models and demonstrated that diabetes incidence rate in the USA has increased with higher outdoor temperatures from 1996 and 2009, after adjustment for most common confounders. They also evidenced an independent association between the prevalence of glucose intolerance worldwide and mean annual temperature on a global scale. The theoretical background for the work mainly stands on the reduction in brown adipose tissue activity due to high ambient temperature that is expected to negatively impact glucose metabolism. This view is plausible, particularly since recent data uncovered potential crosstalk between brown adipose tissue and glucose regulatory pathways,2 but it is important for us to discuss the context of the study.

    We are definitely concerned about the burden of consequences of climate change including biodiversity assault, threats to the human species’ safety, health and well-being because of increased risks related to extreme weather events, wildfire, air quality, and other environmental disease carriers. However, isn’t it cynical that the glucose metabolism disturbance observed in warm environmental temperature might become a serious working hypothesis concomitantly with (b...

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  • Methodological considerations of a systematic review and meta-analysis: dietary carbohydrate restriction in patients with type 2 diabetes

    Thank you to the authors for addressing a relevant and interesting area of research (Snorgaard et al., 2017).

    The review was well planned, but the methodology lacks detail that enables the reader to understand the processes involved in the completion of the meta-analysis and some study limitations were not described.

    Please could the authors clarify why the meta-analyses use both mean change from baseline and mean final value in the same meta-analysis (see Figure 2 and Figure 3 where the lower means indicate change from baseline and the higher means indicate unadjusted final values)? Also, could it be clarified why the selected arms from the three-arm trials were chosen over the arms that were omitted? Although the population, intervention and outcomes were defined in the methodology, the comparator was not.

    Furthermore, when using the mean final HbA1c value in the meta-analyses, papers such as Krebs et al. (2012) and Guldbrand et al. (2012) have higher baseline HbA1cs in the lower-carbohydrate group, which was not mentioned in the paper, nor mentioned as a limitation to the meta-analysis. Guldbrand et al. (2012) demonstrate that HbA1c remained the same at two years (the time point the authors refer to) in the lower-carbohydrate arm but increased in the comparator arm by 0.2%. Therefore the low-carbohydrate arm was the superior intervention; however, the forest plot (Figure 3) suggests that the control intervention was slightly but not significant...

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  • Re:The genes associated with a high risk of type 1 diabetes are becoming less common
    Wen-Peng You
    We thank colleagues for their critical comments that help to clarify relationships we have studied. We are not concerned with the frequency of what specific genes, high-risk or not, has increased recently. We are just making a general statement that with relaxed natural selection detrimental mutations may accumulate. The paper by Witas et al. cited by our critics uses the same rationale as we do when suggesting changes in type 1 d...
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