Leptin

Discussion in 'Diet, Nutrition and Supplements' started by Blondell, May 27, 2006.

  1. Blondell

    Blondell Former Postwhore

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    Leptin: The Next Big Thing
    By Par Deus

    An Introduction to Leptin
    Part I


    Introduction


    Most of you have probably not yet heard of leptin, and, unless you follow the MFW newsgroup, even if you have heard it mentioned somewhere, you probably have no idea of its profound significance in the manipulation of body composition. You soon will.

    I would expect that within a year, it will be everywhere in the bodybuilding world, and within two, it will be the topic of infomercials. It will be bigger than Atkins/ketogenic diets, and bigger than The Zone. When it comes to body composition, this is THE master hormone that controls almost all of the others. It is the reason that prolonged dieting causes fat loss to stop and the main reason overfeeding helps us gain muscle.

    I would love to say "you heard it here first" but I must give credit where credit is due. Lyle McDonald discovered its supreme importance for bodybuilding in the summer of 2000. I had it on my "to do" list at the time because it kept popping up in any research I did on fat loss, but it was not a priority. Lyle, in a moment of ill-advised excuuberance over his discovery made a couple of posts on MFW mentioning it -- and, because I consider him to have the best combination of knowledge and mind in this field, it immediately moved to the top of my list. I believe he communicated his thoughts on its importance to Elzi Volk at the time, but she dismissed it somewhat for a period, so I think it is accurate to say I was the second person to really look into it.

    With that aisde, let us get down to business. This will be the first part of a several part series -- probably at least 4 or 5 -- as this is a massively complicated subject. The present article will be a mere introduction, just to give you some idea of how important this hormone is and how widespread its actions are. In later articles we will delve much deeper into the subject -- from the hard-core, basic science, to the real-world ways in which we can manipulate leptin levels through alterations our diet and supplementation.


    And, I promise the follow-up articles will not be delayed to the same extent that this third issue has been :)




    Background



    In 1953, Kennedy (1) proposed the existence of a centrally acting lipostatic negative feedback signal, produced by adipocytes, in proportion to triacylglycerol content, which regulated body stores via alterations in food intake and energy expenditure -- thus the adipostatic model of weight regulation (aka the "Set-point" theory) was born.

    Strong evidence in favor of this idea came with the discovery of the mutation obese (ob) in mice, which led to early onset of obesity (2), and the subsequent use of parabiosis studies (shared blood supply between two organisms) in the late 60's and early 70's which found that overfeeding of one of the pair, led to decreased food intake in the other (3,4).

    In 1994, the ob gene was cloned and found to code for a 16 kDa protein which was termed "Leptin" from the Greek "leptos", meaning "thin" (5,6). Leptin was the long-sought lipostatic signal and was anointed as the magic bullet that would vanquish obesity. However, this would not be the case, for reasons you will soon learn, and leptin quickly fell off the public map.

    Though, it has remained out of the public eye, a huge amount of research has continued on the subject (and as usual, most of the researchers have shown a gross lack of understanding of leptin -- though of late a few do seem to be getting it, and a huge number of good reviews have been published in the last 2 years.) -- and, though there are numerous unanswered questions, there is enough data to formulate a pretty thorough understanding.



    Physiology


    Leptin belongs, structurally, to the cytokine family (7) -- which includes interleukin-2 (IL-2), interleukin-12 (IL-12), and growth hormone (GH) -- and is synthesized primarily in adipose tissue, with minor contribution coming from gastric mucosa, skeletal muscle (8), and possibly the brain (9). In mice, mutations of the ob gene (and subsequent lack of leptin production) cause early and rapid onset of obesity -- However, this mutation is quite rare in humans (10).

    In human obesity, rather than being absent, serum leptin levels are actually significantly elevated -- Leptin is thought to primarily exert its effects on food intake and energy expenditure, centrally, in the hypothalamus (11,12) -- thus, pointing to a defect in leptin sensitivity. For simplicity's sake, we will use the terms "sensitivity" (as well as "resistance") as encompassing problems in transport accross the Blood Brain Barrier (BBB), receptor issues, and post-receptor signalling issues.

    Numerous factors alter leptin synthesis and secretion, as well as leptin sensitivity including genetics, various nutrients, sex hormones, insulin, catecholamines, fat free mass, fat stores, and energy balance (8, 13, 14). Within an individual, the two most important factors are fat stores, with both fat cell size and fat cell number being positively correlated with leptin levels (15,16), and energy balance -- a negative energy balance, either through fasting or exercise causes a fall in leptin levels, while a positive energy balance, with glucose metabolism being of particular importance (17), causes a rise in leptin levels (8,13). Thus, leptin levels, (and consequently, bodyweight) is regulated in both the short and long-term.

    Factors contributing to leptin resistence are less well understood. This is not a big deal for the dieting bodybuilder with low bodyfat levels as leptin resistance is not the issue, but it has been considerably problematic for the pharmaceutical industry and its plans for leptin as an anti-obesity wonder drug.

    It is not known to what extent poor BBB transport is responsible for obesity and to what extent obesity is responsible for poor BBB transport, but it is known that the obese demonstrate an elevated serum to brain leptin ratio vs. the non-obese (18), that the serum levels are well over the transport saturation point (19), and that elevated leptin levels downregulates leptin transport (20).

    Another possibility is that leptin reaches the brain via the cerebrospinal fluid (CSF), and indeed CSF leptin levels were found to be identical in the obese and non-obese despite drastic differences in serum levels (21).

    There exist at least 6 isoforms of the leptin receptor (21b), with Ob-Rb (long form) being the only one capable of activating signal transduction (22). The purpose of the other five is not fully understood. Alterations in Ob-Rb expression is likely to be a contrubutor as mutations causes obesity in mice (23), and, while this condition is rare in humans (24), elevated leptin levels have been shown to downregulate Ob-Rb expression (25). Ob-Rb is present in the hypothalamic region of the brain where it signals various mediators such as Neuropeptide-Y (NPY), proopiomelanocortin (POMC), and ultimately, the sympathetic nervous system, which in turn alters food intake and energy expenditure (26).

    Another likely possibility for leptin sensitivity problems is post-receptor signalling. SOCS-3, a member of the supressor of cytokine signalling family, is known to inhibit leptin signalling, and upregulation of its activity has been seen following leptin exposure. Thus, it likely acts as a negative feedback mechanism (27, 28).



    Fat Loss


    As mentioned, when it was discovered, leptin was considered an anti-obesity hormone (29). Its administration to rats decreased food intake and increased energy expenditure, causing rapid weight loss, which, unlike starvation, was confined to adipose tissue -- lean mass was preserved (30). It appeared the perfect diet drug had been discovered.

    However, it soon became apparent that humans actually exhibited ELEVATED leptin levels (31), thus not only was exogenously administered leptin ineffective as a diet drug, but endogenous leptin was ineffective as an anti-obesity hormone (32). Thus, the view of leptin's roles has shifted, and leptin is now considered an anti-starvation hormone (33). Though, it is a lack of leptin, not leptin itself that sends the starvation signal. This is where it becomes so very important to bodybuilders.

    Anyone who has dieted for an extended period of time has experienced "hitting the wall", the dreaded slowing and even complete stoppage of fat loss. Perhaps less noticeable, due to the often fanatical will-power of bodybuilders (or perhaps the fanatical use of EC :), is the accompanying increase in true cravings for food. How about increased loss of muscle... And susceptibility to illness... And fatigue...


    This is leptin.


    As briefly mentioned, leptin's actions are controlled primarily by various neuropeptide systems in the hypothalamus, we will get into a bit more detail on the individual mediators involved, below, but for now we will focus on the overall effects produced by elevated and lowered leptin levels.



    Appetite


    Most people have noticed that a diet usually starts out quite easy -- particularly if one is fat or has been on a mass phase for an extended period. However, as the duration of the diet is extended, cravings start to set in and become more and more intense. It has long been recommended that "cheat" days be employed to prevent this -- the explanation given is generally in terms of mental well-being. However, though it is technically in your head (i.e. in the hypothalamus), this phenomenon is NOT psychological.

    Decreases in leptin are strongly associated with increased voluntary food intake in animals and subjective sensations of hunger in humans, independent of the degree of reductions in food intake (34,35). And, the lower leptin goes, the greater the magnitude. By the same token, The administration of exogenous leptin decreases hunger and food intake in animals with defects in leptin production (36).

    In other words, this is not just a matter of will-power, it is a physiological starvation response.



    Energy Expenditure


    Just as with hunger control, fat loss is remarkably rapid at the beginning of a diet, however, it invariably slows, and if appropriate steps are not taken, it stops. Low leptin levels are correlated with decreases in resting energy expenditure (37, 38, 39), and administration of leptin corrects this in animals with defects in leptin production, as well as preventing or reversing the decline seen with fasting (40).

    It has previously been common practice, when the manifestations of low leptin levels become apparant to the dieter, to cut calories even further, increase aerobics, start munching Cytomel, or all of the above. Unfortunately, this is just going to decrease leptin even more, making things that much worse.

    What you should be doing is the exact opposite. I do not like the term "cheat day" because it implies lack of will-power, so we will reserve them for the glutton. What should be employed is a purposeful, planned REFEED. These should actually be done BEFORE the signs of low leptin become manifest, but until you get a feel for that, it will suffice to use them after.



    The Refeed


    As mentioned, there are numerous factors that determine leptin expression, but an exhaustive presentation is beyond the scope of this part of the article, and will be covered in the succedding months. Instead, we just take a brief look at refeeding.

    The primary determinate of leptin expression is glucose metabolism (41). This gives us a really good idea of the macronutrient profile of our refeed. Fat, fructose, protein, and alcohol do not have the same effect on leptin expression that glucose does.

    Assuming we have not created drastically low leptin levels, our refeed will be between 20 and 50% ABOVE maintenence, for 12-48 hours -- the higher the calories, the shorter the refeed -- there are arguments in support of both. If they are drastically low, 5-7 days of 20% above is recommended. In general, the lower you are below your natural bodyfat setpoint, and the longer or more drastic your diet, the more frequent the refeed.

    Because we are eating above maintence, we are most likely accepting some fat gain (though, if leptin levels are really low, the opposite could very well occur due to increases in metabolic rate as leptin is increased), so we want to get the most bang for our buck. Thus, our primary macronutrient will be carbohydrates that enter the blood as glucose -- this means glucose, glucose polymers such as maltodextrin, and starches. Insulin also potentiates glucose stimulated leptin production (13, 41), thus high GI carbs are most ideal. Protein should be 1g/lb, and a bit of fat and fructose in foods you enjoy is acceptable, but the rest is non-fructose carbohydrates.



    The Fed State


    It is also leptin which is responsible for the anabolic hormonal millieu associated with the so-called "fed state", and the lack thereof during underfeeding (42, 43). Thus, in addition to its supreme importance in our fat loss efforts, it is extremely important in increasing and maintaining muscle mass.

    The reason we lose muscle when dieting, despite resistence training and adequate protein intake, is hormonal. The reason we cannot gain maximal amounts of muscle without overeating, and thus accepting some fat gain, is hormonal. And, with the exception of insulin, leptin controls these anabolic hormones -- and both insulin and leptin are mediated by glucose, thus they go hand in hand.

    Increased leptin leads to preferential refilling of liver glycogen stores (44), a prime indicator of the fed state (45). It increases LH which leads to increased testosterone (46). It increases growth hormone (47), it increases t3 (42), and possibly the activity of IGF-1 (48,49). It also blunts ACTH (the hormone that signals cortisol secretion in the adrenals) (50), as well as inhibitng cortisol synthesis directly (51).

    Adequate leptin levels are also necessary for reproduction (52) -- in times of scarcity, when pregancy and another mouth to feed are obviously not a good thing, the reproductive functions of both males and females cease. For males, this goes hand in hand with the drop in testosterone we mentioned, and in women, this is responsible for the loss of menstrual cycles often seen in athletes at low bodyfat levels (53).



    Immune System


    Leptin also mediates the immune suppression seen with fasting and dieting through its direct regulation of T lymphocytes and cytokine production, as well as the activation of monocytes/macrophages (54). Alterations in immune responses are present in leptin-, or leptin-receptor, deficient animals (55). In addition, leptin replacement reverses the immunosuppressive effects of acute starvation in mice (56).



    Nutrients


    There are numerous nutrients which have been shown to positively modulate leptin levels or sensitivity -- many of which are freely available as dietary supplements, some of which are not, and most of which are certainly not being strategically utilized for this purpose. Vitamin E (57), Zinc (58) (400-1200 iu and 25-50mg/day, respectively) and nicotine (59) are three that you can throw into the mix now, an exhaustive presentation will be forthcoming.



    Beyond Leptin


    Though leptin is the master hormone, there are numerous other signals involved in adipostatic control -- and this is where it REALLY gets complicated. Some of these signals are directly modulated by leptin (anorexic peptides are increased, orexigenic are decreased), and some are not. Some are redundant (meaning if they are taken out of the equation, something else takes over) others are not. At last count, there were about 15 of them -- cortisol, gherelin, Neuropeptide-Y, Orexigen a & b, melanin concenrating hormone, cotropin-releasing hormone, and agouti-related peptide are a few that come to mind -- and there are almost certainly many more that we are not yet aware of.


    Next month we will take a closer look at the physiology of leptin, leptin transport, and the leptin receptor.



    Questions and comments on this article can be sent to ParDeus@avantlabs.com


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    29. Spiegelman BM, Flier JS. Adipogenesis and obesity: rounding out the big picture. Cell 1996 Nov 1;87(3):377-89

    30. Halaas JL, Boozer C, Blair-West J, Fidahusein N, Denton DA, Friedman JM. Physiological response to long-term peripheral and central leptin infusion in lean and obese mice. Proc Natl Acad Sci U S A 1997 Aug 5;94(16):8878-83

    31. Maffei M, Halaas J, Ravussin E, Pratley RE, Lee GH, Zhang Y, Fei H, Kim S, Lallone R, Ranganathan S, et al. Leptin levels in human and rodent: measurement of plasma leptin and ob RNA in obese and weight-reduced subjects. Nat Med 1995 Nov;1(11):1155-61

    32. Frederich RC, Hamann A, Anderson S, Lollmann B, Lowell BB, Flier JS. Nat Med 1995 Dec;1(12):1311-4 Leptin levels reflect body lipid content in mice: evidence for diet-induced resistance to leptin action.

    33. Unger RH. Leptin physiology: a second look. Regul Pept 2000 Aug 25;92(1-3):87-95

    34. Brunner L, Nick HP, Cumin F, et al. Leptin is a physiologically important regulator of food intake. Int J Obes Relat Metab Disord 1997;21:1152–60.

    35. Keim NL, Stern JS, Havel PJ. Relation between circulating leptin concentrations and appetite during a prolonged, moderate energy deficit in women. Am J Clin Nutr 1998 Oct;68(4):794-801

    36. Campfield LA, Smith FJ, Guisez Y, Devos R, Burn P. Recombinant mouse OB protein: evidence for a peripheral signal linking adiposity and central neural networks. Science 1995 Jul 28;269(5223):546-9

    37. Doring H, Schwarzer K, Nuesslein-Hildesheim B, Schmidt I. Leptin selectively increases energy expenditure of food-restricted lean mice. Int J Obes Relat Metab Disord 1998 Feb;22(2):83-8

    38. Pelleymounter MA, Cullen MJ, Baker MB, Hecht R, Winters D, Boone T, Collins F. Effects of the obese gene product on body weight regulation in ob/ob mice. Science 1995 Jul 28;269(5223):540-3

    39. Doucet E, St Pierre S, Almeras N, Mauriege P, Richard D, Tremblay A. Changes in energy expenditure and substrate oxidation resulting from weight loss in obese men and women: is there an important contribution of leptin? J Clin Endocrinol Metab 2000 Apr;85(4):1550-6

    40. Scarpace PJ, Matheny M, Pollock BH, Tumer N. Am J Physiol 1997 Leptin increases uncoupling protein expression and energy expenditure. Jul;273(1 Pt 1):E226-30

    41. Mueller WM, Gregoire FM, Stanhope KL, Mobbs CV, Mizuno TM, Warden CH, Stern JS, Havel PJ. Evidence that glucose metabolism regulates leptin secretion from cultured rat adipocytes. Endocrinology 1998 Feb;139(2):551-8

    42. Ahima RS, Prabakaran D, Mantzoros C, Qu D, Lowell B, Maratos-Flier E, Flier JS. Role of leptin in the neuroendocrine response to fasting. Nature 1996 Jul 18;382(6588):250-2

    43. Yu WH, Kimura M, Walczewska A, Karanth S, McCann SM. Role of leptin in hypothalamic-pituitary function. Proc Natl Acad Sci U S A 1997 Feb 4;94(3):1023-8

    44. O'Doherty RM, Anderson PR, Zhao AZ, Bornfeldt KE, Newgard CB Sparing effect of leptin on liver glycogen stores in rats during the fed-to-fasted transition. Am J Physiol 1999 Sep;277(3 Pt 1):E544-50

    45. Lombardo YB, Hron WT, Sobocinski KA, Menahan LA. A metabolic profile of fed and fasting genetically obese mice at 4-5 months of age. Horm Metab Res 1984 Dec;16 Suppl 1:37-42

    46. Finn PD, Cunningham MJ, Pau KY, Spies HG, Clifton DK, Steiner RA.The stimulatory effect of leptin on the neuroendocrine reproductive axis of the monkey. Endocrinology 1998 Nov;139(11):4652-62

    47. Nagatani S, Zeng Y, Keisler DH, Foster DL, Jaffe CA. Leptin regulates pulsatile luteinizing hormone and growth hormone secretion in the sheep. Endocrinology 2000 Nov;141(11):3965-75

    48. Gregoire Nyomba BL, Johnson M, Berard L, Murphy LJ. Relationship between serum leptin and the insulin-like growth factor-I system in humans. Metabolism 1999 Jul;48(7):840-4

    49. Villafuerte BC, Fine JB, Bai Y, Zhao W, Fleming S, DiGirolamo M. Expressions of leptin and insulin-like growth factor-I are highly correlated and region-specific in adipose tissue of growing rats. Obes Res 2000 Dec;8(9):646-55

    50. Heiman ML, Ahima RS, Craft LS, Schoner B, Stephens TW, Flier JS. Leptin inhibition of the hypothalamic-pituitary-adrenal axis in response to stress. Endocrinology 1997 Sep;138(9):3859-63

    51. Pralong FP, Roduit R, Waeber G, Castillo E, Mosimann F, Thorens B, Gaillard RC. Leptin inhibits directly glucocorticoid secretion by normal human and rat adrenal gland. Endocrinology 1998 Oct;139(10):4264-8

    52. Chehab FF, Lim ME, Lu R. Correction of the sterility defect in homozygous obese female mice by treatment with the human recombinant leptin. Nat Genet 1996 Mar;12(3):318-20

    53. Laughlin GA, Yen SS. Hypoleptinemia in women athletes: absence of a diurnal rhythm with amenorrhea. J Clin Endocrinol Metab 1997 Jan;82(1):318-21

    54. Fantuzzi G, Faggioni R. Leptin in the regulation of immunity, inflammation, and hematopoiesis. J Leukoc Biol 2000 Oct;68(4):437-46

    55. Loffreda S, Yang SQ, Lin HZ, Karp CL, Brengman ML, Wang DJ, Klein AS, Bulkley GB, Bao C, Noble PW, Lane MD, Diehl AM. Leptin regulates proinflammatory immune responses. FASEB J 1998 Jan;12(1):57-65

    56. Lord GM, Matarese G, Howard JK, Baker RJ, Bloom SR, Lechler RI. Leptin modulates the T-cell immune response and reverses starvation-induced immunosuppression. Nature 1998 Aug 27;394(6696):897-901

    57. Chen MD, Song YM, Lin PY. Zinc may be a mediator of leptin production in humans. Life Sci 2000 Apr 21;66(22):2143-9

    58. Isermann B, Bierhaus A, Tritschler H, Ziegler R, Nawroth PP. alpha-Tocopherol induces leptin expression in healthy individuals and in vitro. Diabetes Care 1999 Jul;22(7):1227-8

    59. Eliasson B, Smith U. Leptin levels in smokers and long-term users of nicotine gum. Eur J Clin Invest 1999 Feb;29(2):145-52




    Big Motherfucker magazine is a division of Par Deus, Inc.
    ©2000 — 2001. Par Deus, Inc. All Rights Reserved.
     
  2. Jen

    Jen Well-Known Member

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    have always loved this article :cool:
     
  3. Blondell

    Blondell Former Postwhore

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    I've fallen in love w/ it myself. It's very informative. :)
     
  4. GraceGirl

    GraceGirl His Beautiful Paradox

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    Yes, I concur. A great read. :banana:
     
  5. Tearose

    Tearose Focused and On Fire

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    wow, I want to read the next one.
     
  6. jrb1980

    jrb1980 Well-Known Member

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    where is it from Blondell? do you have a link?
     
  7. Blondell

    Blondell Former Postwhore

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  8. jrb1990 Roommate

    jrb1990 Roommate New Member

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    Thanks babe. J. :hi:
     
  9. Lynny

    Lynny I like me.

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    Man, that is so interesting. thanks for posting that!!
     
  10. homeschoolmom

    homeschoolmom Well-Known Member

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    Great article! Now I have a better understanding of the purpose of refeeds which I hadn't understood very well before this. Thanks for posting this. :)
     
  11. rachel.

    rachel. EP Boardoholic

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    So in essence, they are suggesting to take 1-2 weeks caloric intake above maintenance to promote greater fat loss by "fixing" the leptin levels in the body?
     
  12. Blondell

    Blondell Former Postwhore

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  13. sunny

    sunny Member

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  14. funnyesq

    funnyesq Member

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    Can someone please help with HOW do I determine the amount and WHEN to "refeed?" All I got is 20-50% above maintenance but nothing about "timing" etc. How often? It could be for up to 48 hours...but how do I determine how long? If it helps, I'm 5'8" currently about 159 lbs and probably about 35% BF I'm on a calorie deficit of about 1500 calories a day with about 120 grms protein, 35 grams of fat (fish oil, etc....i.e. healthy fats) and the rest in carbs which include veggies (fibrous) and fruit (fibrous i.e. strawberries and/or pineapple and/or blueberries). The 1500 seems to be as high as I can go and still lose fat/weight. I have mostly a desk job and my main "movement" is working out 4-5 days a week which include some cardio and some Yoga as well as Weight lifting 4-5 times a week. Help?
     
  15. JJ29

    JJ29 BBB member

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    Start with a 5 hour refeed every 7 days and see how your body reacts.
     
  16. sunny

    sunny Member

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    Berardi on refeeds (2003):

    Q: Do you believe that refeeds should be administered to increase leptin levels and why?

    A: Lyle McDonald (more of a leptin expert than I’ll ever be) and I just had a discussion about this with David Greenwalt and his coaching group over at leannesslifestyle.com and we both pretty much concluded that refeeds probably won’t do much for dieters in terms of leptin. For starters, leptin kicks up and down very rapidly as energy intake fluctuates. Therefore, while leptin may kick up with a 10-hour carbohydrate reefed, it’s likely to drop back down just as rapidly after the reefed is over and another 10 hours of dieting are accomplished. Therefore, a dieter may just end up with a bigger positive energy balance during those 24hours of refeeding and subsequent return to dieting.

    Since there is no data, one way or the other, illustrating what happens in dieting weight lifters when refeeding, there's only speculation. Of course, leptin itself aside, if there were some prolonged increase in leptin, we should be able to measure the effects of this leptin increase by observing increases in metabolic rate the day after the refeed. Unfortunately, metabolic increases as a result of acute overfeeding aren’t observed a day after the overfeed (or refeed). Remember, we’re not so much interested in what’s happening with leptin itself but what’s happening to metabolism. Leptin doesn’t impact fat loss. The effects of leptin do. And it doesn’t appear that refeeds impact metabolism for any longer than the day of the refeed.

    However, make no mistake about it. I am not saying that refeeds are useless. In fact, I do see other good reasons (i.e. a psychological break from dieting, increased adherence, better glycogen status, more intense workouts, suppression of the catabolic hormonal cascade associated with dieting) for refeeding besides the leptin issue. A common strategy that I use with dieting bodybuilders is to have them do a 1-day refeed once per week. This refeed usually contains 50% - 100% more energy than their daily intake from the other 6 days. Therefore if the bodybuilder is eating 1000 kcal per day, he/she will refeed on 1500 – 2000 kcal. Likewise, if the bodybuilder is eating 2000 kcal per day, he/she will refeed on 3000 – 4000 kcal. The magnitude of the re-feed is dependent on their leanness, on how low their energy intake is, and on their rate of fat loss.

    In addition to this refeeding on the micro- scale, I will usually have the same bodybuilder re-feed on a macro- scale by eating 50% - 100% more energy for a full week after every 4 – 6 weeks of dieting. The frequency and size of this macro- refeed is dependent again on the bodybuilder’s leanness, on how low their energy intake is, and on their rate of fat loss. You can think of this refeeding strategy as calorie periodization. We do it for training, why not for nutrition?

    While I have just discussed my strategies for dieting bodybuilders, I use similar strategies for most of my other athletes as well, especially the ones trying to maximize their power to weight ratios. In these athletes, however, their calories are cycled according to their recovery needs. On hard days the calories are higher while on easy days the calories are lower. Refeed weeks are used when performance starts to suffer or when fat loss slows.
     
  17. Blondell

    Blondell Former Postwhore

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    That's good info. Do you have the link?
     
  18. sunny

    sunny Member

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    Berardi on refeeds (2003)

    Probably, with refeeds one should experiment - once you feel constantly tired, weak and lethargic at the gym, you might consider refeeding more often.
     
  19. rachel.

    rachel. EP Boardoholic

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    As a personal story, I would highly recommend refeeds.

    Although I gotta admit, it was more an accident but in any case a large carb load for the day and I felt 100 times better the next day at the gym. A lot more energy to increase my weights :cool:
     
  20. PowerManDL

    PowerManDL Banned

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    I tend to refeed at least once a week regardless. Usually Saturday, and sometimes Sunday, are just "eat what I want" days. Typically a lot of junk food.
     

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