Skip Breakfast – Lose Weight

Skip Breakfast

Skip Breakfast

** Let me first just say, the premise of this article is gleaned from the work of Kiefer @ – I highly suggest heading over there for much more quality content.

Yes, basically it’s like this:

We have two exceptionally important hormones waging wars and construction projects all day and night long.

These two hormones:  1.  Insulin   2.  Cortisol

Insulin signals cells to shuttle all kinds of nutrients and building blocks across the cellular wall.

Cortisol catabolizes body tissue, which can include muscle, but only if certain signals in the body direct it to do so.

Insulin and Cortisol dip and dive with highs and lows based upon specific circadian rhythms.    Insulin is most sensitive in the morning time and its sensitivity basically dissipates as the day continues. There is no disputing that insulin sensitivity is highest in the morning and early afternoon, and by evening, sensitivity is significantly blunted. Cortisol levels naturally rise through the evening and peak around wake-up time.

High Cortisol, High Insulin = FAT

The resulting hormonal cocktail, particularly the simultaneously elevated cortisol and insulin, conspires to make you fat.

Cortisol, normally thought of as a catabolic agent with regards to muscle, breaks down body fat when insulin levels are low (e.g. Not eating in the morning), which means elevated cortisol levels in the morning equates to a monster fat burner window. Accelerated fat burning lasts all morning…unless you introduce specific macronutrients in specific doses, which invariably will antagonize insulin sensitivity; raising insulin levels.

If cortisol acts alone, in the absence of insulin, it forces the body to preferentially burn body fat; this is the exact scenario you find yourself in upon waking; that is, if you don’t screw it up by eating carbs. And if you don’t eat anything, or better yet appropriately select quality fats for morning intake, cortisol continues signaling the release of body fat for metabolism, just as it did through the previous hours of snoozing.  THIS IS YOUR GOLDEN WINDOW.

There’s another problem with high insulin levels plus high cortisol levels. When the two are elevated together, the body gets another signal: start making as many new, empty fat cells as possible—the max number of which being determined by how much body fat you already have stored, the more fat, the more empty fat cells created.

Low insulin levels, which occur in the absence of dietary carbohydrates, can accelerate the release of fatty acids, and increase lipolysis (fat-burning).

Studies also show that eating more food in the beginning of the day when sensitivity is high causes more muscle than fat to be lost during dieting, but that eating most of your calories in the evening causes the loss of body fat and the preservation of muscle.

Couple other cool notes:

Ghrelin, another hormone that you’ll find aggravating you in the morning, causing your stomach to growl; sparking hunger, also stimulates growth hormone release ,which in turn, ignites more fat burning! Hunger and fat burning go hand in hand first thing in the morning.

Eating breakfast can reduce fat burning for the entire rest of the day, and while cortisol levels remain high, the insulin release causes new empty fat cells to be created. As the insulin continues to rise, growth hormone subsides and body‐fat burning grinds to a halt.

The central nervous system also functions with greater efficiency when not shifted from equilibrium with food. Without the morning disruption of food, motor signals from the central nervous system (CNS) increase in amplitude, allowing an increase in single‐rep power production, and fine‐motor control.

Another Note: Training without breakfast doubles the growth response compared to training on a full stomach.

That’s enough to “digest” for now.  For a more thorough, comprehensive detailing of the necessity of skipping breakfast and how it relates to an overall kick ass nutritional/training strategy, check out my boy Kiefer’s website:  DangerouslyHardcore.

References:  (Sorry they are not in order or properly cited after the relevant material)

Owen OE, Cahill GF. 1973 Metabolic effects of exogenous glucocorticoids in
fasted man. J Clin Invest. 52:2596 –2605.

De Bock K, Richter EA, Russell AP, Eijnde BO, Derave W, Ramaekers M, Koninckx E, Léger B, Verhaeghe J, Hespel P. Exercise in the fasted state facilitates fibre type-specific intramyocellular lipid breakdown and stimulates glycogen resynthesis in humans. J Physiol. 2005 Apr 15;564(Pt 2):649-60.

Van Loon LJ, Koopman R, Stegen JH, Wagenmakers AJ, Keizer HA, Saris WH. Intramyocellular lipids form an important substrate source during moderate intensity exercise in endurance-trained males in a fasted state. J Physiol. 2003 Dec 1;553(Pt 2):611-25. Epub 2003 Sep 26.

Van Proeyen K, Deldique L, Nielens H, Szlufcik K, Francaux M, Ramaekers M, Hespel P. Effects Of Training In The Fasted State In Conjunction With Fat-rich diet On Muscle Metabolism: 721: June 3 8:15 AM – 8:30 AM. Medicine & Science in Sports & Exercise. 42(5):42, May 2010.

De Bock K, Richter EA, Russell AP, Eijnde BO, Derave W, Ramaekers M, Koninckx E, Léger B, Verhaeghe J, Hespel P. Exercise in the fasted state facilitates fibre type-specific intramyocellular lipid breakdown and stimulates glycogen resynthesis in humans. J Physiol. 2005 Apr 15;564(Pt 2):649-60.

More just breakfast specific:

Martin A, Normand S, Sothier M, Peyrat J, Louche-Pelissier C, Laville M. Is advice for breakfast consumption justified? Results from a short-term dietary and metabolic experiment in young healthy men. Br J Nutr. 2000 Sep;84(3):337-44.

Broglio F, Benso A, Gottero C, Prodam F, Grottoli S, Tassone F, Maccario M, Casanueva FF, Dieguez C, Deghenghi R, Ghigo E, Arvat E. Effects of glucose, free fatty acids or arginine load on the GH-releasing activity of ghrelin in humans. Clin Endocrinol (Oxf). 2002 Aug;57(2):265-71.

Super great read on Cortisol and GH and it’s affect on lipolysis (fat-burning)

Effects of Cortisol and Growth Hormone on Lipolysis in Human Adipose Tissue*
MALIN OTTOSSON, PETER LO¨ NNROTH, PER BJO¨ RNTORP, AND STAFFAN EDE´N Wallenberg Laboratory for Cardiovascular Research, Department of Physiology and Pharmacology,
Endocrine Unit (M.O., S.E.), Department of Internal Medicine (P.L.), and Department of Heart and Lung Diseases (P.B.), Sahlgrenska University Hospital, Goteborg University, Goteborg, Sweden

Dinneen S, Alzaid A, Miles J, Rizza R. Effects of the normal nocturnal rise in cortisol on carbohydrate and fat metabolism in IDDM. Am J Physiol. 1995 Apr;268(4 Pt 1):E595-603.

Samra JS, Clark ML, Humphreys SM, Macdonald IA, Matthews DR, Frayn KN. Effects of morning rise in cortisol concentration on regulation of lipolysis in subcutaneous adipose tissue. Am J Physiol. 1996 Dec;271(6 Pt 1):E996-1002.

Trumper BG, Reschke K, Molling J. Circadian variation of insulin requirement in insulin dependent diabetes mellitus the relationship between circadian change in insulin demand and diurnal patterns of growth hormone, cortisol and glucagon during euglycemia. Horm Metab Res. 1995 Mar;27(3):141-7.

Schmidt-Reinwald A, Pruessner JC, Hellhammer DH, Federenko I, Rohleder N, Schurmeyer TH, Kirschbaum C. The cortisol response to awakening in relation to different challenge tests and a 12-hour cortisol rhythm. Life Sci. 1999;64(18):1653-60.
Rise and Fall – Cicadian rhythms of Cortisol

Doman J, Thompson S, Grochocinski V, Jarrett D, Kupfer DJ. A computer algorithm to determine the nadir and rise time in nocturnal cortisol secretion. Psychoneuroendocrinology. 1986;11(3):359-66.

Fain JN. Inhibition of glucose transport in fat cells and activation of lipolysis by glucocorticoids. In: Baxter JD, Rousseau GG, eds. Glucocorticoid hormone action. Berlin, Heidelberg, New York 1979:Springer-Verlag;547-560.

Dinneen S, Alzaid A, Miles J, Rizza R. Metabolic effects of the nocturnal rise in cortisol on carbohydrate metabolism in normal humans. J Clin Invest. 1993 Nov;92(5):2283-90.
Divertie GD, Jensen MD, Miles JM. Stimulation of lipolysis in humans by physiological hypercortisolemia. Diabetes. 1991 Oct;40(10):1228-32.

Gravholt CH, Dall R, Christiansen JS, Moller N, Schmitz O. Preferential stimulation of abdominal subcutaneous lipolysis after prednisolone exposure in humans. Obes Res. 2002 Aug;10(8):774-81.

Djurhuus CB, Gravholt CH, Nielsen S, Mengel A, Christiansen JS, Schmitz OE, Moller N. Effects of cortisol on lipolysis and regional interstitial glycerol levels in humans. Am J Physiol Endocrinol Metab. 2002 Jul;283(1):E172-7.

Djurhuus CB, Gravholt CH, Nielsen S, Pedersen SB, Moller N, Schmitz O. Additive effects of cortisol and growth hormone on regional and systemic lipolysis in humans. Am J Physiol Endocrinol Metab. 2004 Mar;286(3):E488-94.
Hirsh E, Halberg F, Goetz FC, Cressey D, Wendt H, Sothern R, Haus E, Stoney P, Minors D, Rosen G, Hill B, Hilleren M, Garet K. Body weight change during 1 week on a single daily 2000-calorie meal consumed as breakfast (B) or dinner (D). Chronobiologia 1975;2(suppl 1): 31-32.

Jacobs H, Thompson M, Halberg E, Halberg F, Fraeber C, Levine H, Haus E. Relative body weight loss on limited free-choice meal consumed as breakfast rather than as dinner. Chronobiologia 1975;2(suppl 1): 33.
Sensi S, Capani F. Chronobiological aspects of weight loss in obesity: effects of different meal timing regimens. Chronobiol Int. 1987;4(2):251-61.

Shiiya T, Nakazato M, Mizuta M, Date Y, Mondal MS, Tanaka M, Nozoe S, Hosoda H, Kangawa K, and Matsukura S. Plasma ghrelin levels in lean and obese humans and the effect of glucose on ghrelin secretion. J Clin Endocrinol Metab 87: 240–244, 2002.

Kojima M, Hosoda H, Date Y, Nakazato M, Matsuo H, Kangawa K. Ghrelin is a growth-hormone-releasing acylated peptide from stomach. Nature. 1999 Dec 9;402(6762):656-60.

Takaya K, Ariyasu H, Kanamoto N, Iwakura H, Yoshimoto A, Harada M, Mori K, Komatsu Y, Usui T, Shimatsu A, Ogawa Y, Hosoda K, Akamizu T, Kojima M, Kangawa K, Nakao K. Ghrelin strongly stimulates growth hormone release in humans. J Clin Endocrinol Metab. 2000 Dec;85(12):4908-11.

Hataya Y, Akamizu T, Takaya K, Kanamoto N, Ariyasu H, Saijo M, Moriyama K, Shimatsu A, Kojima M, Kangawa K, Nakao K. A low dose of ghrelin stimulates growth hormone (GH) release synergistically with GH-releasing hormone in humans. J Clin Endocrinol Metab. 2001 Sep;86(9):4552.

Insulin is a potent inhibitor of lipolysis (Vikman, H. L., Ranta, S., Kiviluoto, T., Ohisalo, J. J. (1991) Different metabolic regulation by adenosine in omental and subcutaneous adipose tissue. Acta Physiol Scand 142: 405–410.) and stimulates lipoprotein lipase (LPL), thus, favoring deposition of triglycerides in adipose tissue, whereas cathecolamines, thyronines, and growth hormone (GH) stimulate the release of FFA from adipose tissue. Cathecolamines are very potent physiological stimulators of lipolysis in adipose tissue through stimulatory 1-, 2-, and 3-adrenoreceptors and inhibitory 2-adrenoreceptors (Fain, J. N., Garcia-Sainz, J. A. (1983) Adrenergic regulation of adipocyte metabolism. J Lipid Res 24: 945–966. & Enoksson, S., Shimizu, M., Lonnqvist, F., Nordenstrom, J., Arner, P. (1995) Demonstration of an in vivo functional 3-adrenoceptor in man. J Clin Invest 95: 2239–2245.), and subsequent modulation of the hormone-sensitive lipase.

Hauner H, Schmid P, Pfeiffer EF. Glucocorticoids and insulin promote the differentiation of human adipocyte precursor cells into fat cells. J Clin Endocrinol Metab. 1987 Apr;64(4):832-5.

Vikman, H. L., Ranta, S., Kiviluoto, T., Ohisalo, J. J. (1991) Different metabolic regulation by adenosine in omental and subcutaneous adipose tissue. Acta Physiol Scand 142: 405–410.