Responses

PDF

Parental history of type 2 diabetes is associated with lower resting energy expenditure in normoglycemic subjects
Compose Response

Plain text

  • No HTML tags allowed.
  • Web page addresses and e-mail addresses turn into links automatically.
  • Lines and paragraphs break automatically.
Author Information
First or given name, e.g. 'Peter'.
Your last, or family, name, e.g. 'MacMoody'.
Your email address, e.g. higgs-boson@gmail.com
Your role and/or occupation, e.g. 'Orthopedic Surgeon'.
Your organization or institution (if applicable), e.g. 'Royal Free Hospital'.
Statement of Competing Interests

PLEASE NOTE:

  • Responses are moderated before posting and publication is at the absolute discretion of BMJ, however they are not peer-reviewed
  • Once published, you will not have the right to remove or edit your response. Removal or editing of responses is at BMJ's absolute discretion
  • If patients could recognise themselves, or anyone else could recognise a patient from your description, please obtain the patient's written consent to publication and send them to the editorial office before submitting your response [Patient consent forms]
  • By submitting this response you are agreeing to our full [Response terms and requirements]

Vertical Tabs

Other responses

Jump to comment:

  • Published on:
    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.

    Conflict of Interest:
    None declared.
  • Published on:
    Energy Metabolism, particularly in humans, depends on myriads of food micronutrients - far to complex to quantify
    • Anne-Thea McGill, Human Nutrition Researcher/FRA&NZCsGP Southern Cross University

    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...

    Show More
    Conflict of Interest:
    None declared.
  • Published on:
    The 3500 Kcal Rule is Invalid for Projections of Weight Change
    • Andrew W Brown, Assistant Professor Department of Applied Health Science, Indiana University School of Public Health-Bloomington, Bloomington, IN, USA
    • Other Contributors:
      • Kevin Hall, Section Chief, Integrative Physiology Section, Laboratory of Biological Modeling
      • Steven B Heymsfield, Professor
      • David B Allison, Dean, Distinguished Professor, & Provost Professor

    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...

    Show More
    Conflict of Interest:
    KH receive a patent on a method of personalized dynamic feedback control of body weight, assigned to the National Institutes of Health. AWB and DBA are supported in part by NIH grants R25DK099080 and R25HL124208. The content is solely the responsibility of the authors and does not necessarily represent the official views of the National Institutes of Health or any other organization.