Welcome to Debate Club! Please be aware that this is a space for respectful debate, and that your ideas will be challenged here. Please remember to critique the argument, not the author.

How significant are hormones in appetite control

Options
yarwell
yarwell Posts: 10,477 Member
Recent study from Denmark ( abstract here ) found that it took ~40 weeks for hunger regulating hormone Ghrelin to get back towards its pre-weight loss value having used a VLCD to achieve 13% weight loss in 8 weeks and then support and tracking to maintain the weight loss for a year.

Further info at http://healthsciences.ku.dk/news/new-2016/new-research-obese-people-can-maintain-stable-weight-loss/

This seems to identify a real physical effect (increased hunger) that can be overcome with effort but largely goes away with time as the systems accept the new body weight. If this is repeatable perhaps it would be an objective way to measure the difficulty or otherwise of alternative dieting strategies - for example would a 12 month small deficit progressive weight loss have been easier to manage than losing about 3 lbs/week for 8 weeks and then maintaining.

Thoughts ?

Replies

  • silverkitty777
    silverkitty777 Posts: 10 Member
    Options
    Good question. I will leave an answer soon, as I'm dealing with this now -

    Skeletal muscle as a gene regulatory endocrine organ.
    Karstoft, Kristian; Pedersen, Bente K.

    Current Opinion in Clinical Nutrition & Metabolic Care
    Post Author Corrections: April 20, 2016
    Abstract

    Purpose of review: Skeletal muscle is gaining increased attention as an endocrine organ. Recently, novel myokines and new effects of already established myokines have been identified. The objective of this review is to give an update on the recent advances in the field.

    Recent findings: Several hundred putative myokines have been described, some of which are induced by contraction and differentially regulated between healthy and metabolically diseased individuals. Interleukin-6 (IL-6) is the prototype myokine, which was identified as a muscle-derived cytokine 15 years ago. Recently, IL-6 has been linked to [beta]-cell survival and inhibition of cancer-cell growth. Moreover, trans-signaling appears to determine whether IL-6 acts as a proinflammatory or an anti-inflammatory cytokine. Irisin has been shown to be a secreted myokine, which contribute to circulating concentrations dependent on training status. IL-15 has been established as a cytokine mediating cross-talk between skeletal muscle and skin tissue, and decorin has been characterized as a contraction-induced myokine which apparently is differentially regulated between healthy and dysglycemic individuals.

    Summary: Skeletal muscle is an endocrine organ which, by the release of myokines, may influence metabolism in virtually all organs in the body. This knowledge may potentially open up for the possibility of designing new drugs that mimic the effects of myokine signaling.

    Copyright (C) 2016 Wolters Kluwer Health, Inc. All rights reserved.
  • eburns55555
    eburns55555 Posts: 26 Member
    Options
    This is a great article. Thank you for posting this.
  • GaleHawkins
    GaleHawkins Posts: 8,160 Member
    Options
    Thanks for the article. Having maintained at 200 for over a year now it made me feel good . :)
  • lithezebra
    lithezebra Posts: 3,670 Member
    Options
    Increased hunger goes away with time is the best news I've heard in a long time.
  • GaleHawkins
    GaleHawkins Posts: 8,160 Member
    Options
    @silverkitty777 I was googling 'Skeletal muscle is an endocrine organ' and if nutritional ketosis could pay a role of triggering in of the actions talked about in your link and somehow stumbled into the below link. Two weeks into nutritional ketosis my cravings/hunger faded fast and 20 months later I still have no cravings but I will for some reason reach for a can of tuna (protein) without having planned to eat tuna. @yarwell was talking about the study indicating about 40 weeks Ghrelin to reset (my wording). Set point came to my mind as well. The below may not be related so I do not want to get the thread off track but I expect there is a connect somewhere.

    sciencedirect.com/science/article/pii/S1550413107001374

    "Main Text
    Biology of Fasting

    The adaptation from the fed to fasted (total lack of food intake, usually acute) or starved (chronic undernutrition) state has been a subject of fascination, and investigation, for centuries (Cahill, 2006 and Keys et al., 1950; see also Tucker, 2006). In the fed state, glucose fulfills the body's acute, immediate energy needs. The body senses a drop in glucose concentration at sites such as the pancreatic islets, brain, and portal vein. It responds by reducing insulin secretion from islet β cells and by increasing glucagon secretion from islet α cells. Another response is sympathetic adrenal stimulation causing increased epinephrine levels; this arm is of secondary importance but has a larger role in patients with type 2 diabetes (Cryer et al., 2003).

    During fasting, liver glycogen, a glucose-storage polymer, is initially mobilized to replenish blood glucose (glycogenolysis). Major changes in metabolism occur as the glycogen supply dwindles. Stored adipose tissue triglycerides are released into the circulation as glycerol and fatty acids. The glycerol is converted by the liver into glucose (gluconeogenesis). The fatty acids are directly oxidized as an energy source by some tissues (liver and muscle); the liver also metabolizes the fatty acids to β-hydroxybutyrate and acetoacetate (“ketone bodies”). Ketone bodies are released into the circulation for use by tissues, notably the brain, which cannot use fatty acids. The liver also uses ketones for gluconeogenesis. When fasting is prolonged, muscle protein breakdown occurs, sending alanine to the liver as another substrate for gluconeogenesis (Cahill, 2006)....."
  • kshama2001
    kshama2001 Posts: 27,913 Member
    Options
    yarwell wrote: »
    Recent study from Denmark ( abstract here ) found that it took ~40 weeks for hunger regulating hormone Ghrelin to get back towards its pre-weight loss value having used a VLCD to achieve 13% weight loss in 8 weeks and then support and tracking to maintain the weight loss for a year.

    Further info at http://healthsciences.ku.dk/news/new-2016/new-research-obese-people-can-maintain-stable-weight-loss/

    This seems to identify a real physical effect (increased hunger) that can be overcome with effort but largely goes away with time as the systems accept the new body weight. If this is repeatable perhaps it would be an objective way to measure the difficulty or otherwise of alternative dieting strategies - for example would a 12 month small deficit progressive weight loss have been easier to manage than losing about 3 lbs/week for 8 weeks and then maintaining.

    Thoughts ?

    Well, in my n=1, I lost 30 pounds in a year with hunger only right before meals and consider this to have been easy. I think my conservative goals helped me not go nuts and gain weight over the holidays.
  • beautifulwarrior18
    beautifulwarrior18 Posts: 914 Member
    edited May 2016
    Options
    Well there's one week of every month where I could eat a big, greasy horse and I'd still be hungry, so yeah I'd say they play a very big part.
  • EvgeniZyntx
    EvgeniZyntx Posts: 24,208 Member
    edited May 2016
    Options
    yarwell wrote: »
    Thoughts?

    Clearly hormones play a major role in appetite control, however research still tends to focus either on one hormone or one effect of that hormone where the interplay between hormonal function, diet, physiological response and long term weight loss tends to be poorly described or understood in a manner accessible to the lay population.

    For example, take glp-1, which is mentioned in the paper review, as an appetite inhibitor. It's a molecule involved in insulin and glucagon secretion and is inhibited incredibly fast in the body. There is a lot of research currently related to diabetes.

    It's produced in the gut when we eat and has a rapid role in feeling full. It reduces gastric emptying and ... well, it gets complicated fast.

    vca6two9edy0.png

    (from https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3796262/)

    As important as these mechanisms are and it is interesting to see reports that these change over time - I think that this type of research fails to differentiate on dietary impact.

    Changes in sweetness, fiber content, macros or, even exercise, have an impact on satiety that is probably more immediate than these hormonal "resets", that tend to be long term.

    Which is why, with regards to satiety and hunger, I don't argue against "clean eating" or other WOE that aren't my own. Finding a solution that allows a balance between the cultural environment, taste and calorie restriction has many paths. Eat in a way that makes you feel full with less. The body does adjust satisfaction levels.

    On the other hand, I'm always very suspect when someone focuses on a specific hormone ("it's my *insulin, ghrelin, leptin, dopamine that are all wakadoodle in my fat gain") as the specific issue or solution.

    Short response: hormones are hugely significant in appetite control, in weight loss, it's a personal trial by error to find our what helps manage appetite both short term and long term. Some best practices or general guidelines can be eeked out. I've yet to hear about a method that has significant success rate for "obese-people-can-maintain-stable-weight-loss" as the article title suggests.

    *outside T2DM