The Seven Secrets of Slim People

4. Stop when you are no longer physically hungry, no matter how much food is or is not left on your plate.

Sorry, I was out of touch for a while. I didn't just come in here and "bash" because clearly i stated that it is wrong. To understand why it's wrong you need to understand WHY you feel hungry and the way that your body works. Hunger and Satiety are controlled by two hormones called Leptin and Ghrelin.

Leptin is the hormone in your body that regulates hunger. Leptin production follows caloric intake: if you restrict calories, your Leptin production will decrease and you will feel less hungry. This is how anorexics can eat 800 calories a day and not feel hungry. If you eat more, your Leptin production will increase, and you will feel more hungry.

Because you are restricting calories, your Leptin production is out of whack; meaning, DO NOT listen to your body about how much/when to eat. Get your calories in and your Leptin production will follow, soon it will be no problem.

Additionally these hormones can be affected by- exercise, sleep, weight, body fat, menstruation, etc.

Lastly, the idea that "only eating when you're hungry" has another fatal flaw. It DOES NOT take into account WHAT you are eating. You're hungry and you're going to eat some cheesecake and a bacon ranch cheeseburger until you're no longer hungry? You may have just gone over your calories. You aren't very hungry as your leptin is low so you only ate two meals that totalled 700 calories for the day?

Do you see what i'm getting at? These hormones directly affect your hunger satiety and are not an accurate representation of your nutritional needs. Every been on your period and been RAVENOUS? Ever work out really hard and be RAVENOUS? Ever completely lose hunger when you first start cutting calories?

This is my point. Please feel free to look this up in medical journals or read studies. These are facts and NOT "my opinion".

That's not how it works, there are many more hormones involved. Start here-

Physiology & Behavior
Volume 81, Issue 5, July 2004, Pages 719–733

Proceedings from the 2003 Meeting of the Society for the Study of Ingestive Behavior (SSIB)


Endocrine controls of eating: CCK, leptin, and ghrelin
Nori Geary,
E.W. Bourne Laboratory, Weill Medical College of Cornell University, White Plains, NY 10506, USA
http://dx.doi.org/10.1016/j.physbeh.2004.04.013, How to Cite or Link Using DOI

Abstract
The peripheral physiological and central nervous mechanisms contributing to the control of eating present formidable challenges to experimental analysis. One of the most productive approaches to these challenges has been endocrinological. This review introduces the endocrine control of eating by considering three hormonal signals that have been hypothesized to control hunger or satiation, cholecystokinin CCK, leptin, and ghrelin. The roles of these molecules in humans and in rodents are considered against a set of criteria established in classical endocrinology for establishing physiological endocrine action. It is concluded that according to these criteria, CCK's satiating action in humans is the best-established physiological endocrine action. In contrast, support for endocrine actions of leptin in satiation and of ghrelin in hunger is incomplete, and areas urgently requiring further research are identified. Finally, a review of work on these three hormones suggests the utility of a new conceptual scheme for understanding the endocrine control of eating. This scheme distinguishes between endocrine, in which the stimuli for hormonal secretion and the effect of secretion on eating are tightly coupled, and endocrine effects, in which one or both of these links is uncoupled. The implications of this concept for research design and interpretation of data are discussed.

A vast literature links endocrine systems to the control of eating behavior [Geary, N. Hunger and satiation. In: Martini, L., ed. Encyclopedia of endocrine diseases. San Diego, CA: Academic Press, 2004, in press.]. This is fortunate for ingestive science. Endocrinology is a well-developed discipline with an impressive armamentarium of intellectual and technical tools. In contrast, ingestive science, i.e., the study of eating, drinking, and drug use, is at a more rudimentary stage of development. My general thesis here is that the adaptation and application of some of the well-accepted intellectual tools of endocrinology is likely to accelerate progress in ingestive science.

The organization of the review is threefold. First, the treatment of endocrine controls of eating is selective. Just three hormones, CCK, leptin, and ghrelin, are considered. It is not clear that these are the three most important endocrine controls of eating, but they are each certainly interesting candidates, and comparisons among them are instructive. Second, I argue for the utility of the application of classical endocrine criteria for the identification of physiological effects of hormones, as adapted to eating behavior. This is done by introducing these criteria, considering each hormone's status with respect to them, and identifying the areas where relevant evidence is currently available or is lacking. Third, I argue for the utility of making explicit the distinction between endocrine actions, in which the stimuli for hormonal secretion and the effect of secretion on eating are tightly coupled, and endocrine actions, in which these links are uncoupled. This concept is assembled inductively in the course of the review.

Keywords
Endocrine controls; CCK; Leptin; Ghrelin
Figures and tables from this article:


Fig. 1. Endocrine action of CCK on gall bladder contraction in humans. Top panel: Ingestion of a meal elicits an increase in plasma CCK concentration and is associated with the contraction of the gall bladder. Middle panel: Intravenous infusion of 0.2 pMol/kg/min CCK-8 mimics the initial prandial increase in plasma CCK and is sufficient to produce normal prandial gall bladder contraction in men. Bottom panel: Oral administration of 10 mg of the CCK1R antagonist devazepide during the meal prevents prandial gall bladder contraction. Upper and middle panels are from Ref. [52]; lower panel is from Ref. [51]; used with permission.
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Fig. 2. The CCK1R antagonist loxiglumide antagonizes the satiation action of endogenous CCK in humans. Top panel: Loxiglumide blocks the satiating action of endogenous CCK stimulated by intraduodenal infusion of fat emulsion. Normal-weight adult males began a noontime lunch buffet 4 h after a standard breakfast, 90 min after beginning an intravenous infusion of loxiglumide (10 μmol/kg-h) or saline, 60 min after an intraduodenal infusion of corn oil or saline (0.4 ml/min), and 20 min after an oral preload of 400 ml of a low-fat banana milkshake. The infusions were continued throughout the meal. Intraduodenal fat infusion significantly reduced the size of the lunch meal (expressed as total energy content of the various foods) without producing physical or subjective side effects, and this inhibition of eating was reversed by loxiglumide infusion. Bottom panel: Loxiglumide stimulates eating. Normal-weight adult males began a noontime lunch buffet 4 h after a standard breakfast and 60 min after beginning an intravenous infusion of loxiglumide (22 μmol/kg-h) or saline. Infusions were continued throughout the meal. Loxiglumide significantly increased meal size without affecting the participants' enjoyment of their meals or their subjective sense of normal satiation. Upper panel is from Ref. [57]; lower panel is from Ref. [10]; used with permission.
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Fig. 3. Superior pancreaticoduodenal (SPD) artery injection of the CCK1R antagonist devazepide stimulates eating in rats at doses that are ineffective when infused via the jugular vein (intraventricular). Injections were done immediately before the 15-min access to 30% sucrose solutions after a 6-h food deprivation during the light phase. The superior pancreaticoduodenal artery perfuses the pyloric region of the stomach and the proximal small intestine. From Ref. [18], used with permission.
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Fig. 4. Endocrine controls may be considered to function through a chain of two stimulus–response links. In the first link, a stimulus for hormone secretion is linked to hormone secretion. In the second link, hormone secretion is the stimulus and eating is the response. Each of these links can be considered tightly coupled (top panel, filled arrows) or uncoupled (bottom panel, unfilled arrows). The first link is coupled when there are discrete, highly time-locked causal physiological cascades between the stimulus for hormone secretion and secretion. Similarly, the second link is coupled when there is a time-locked causal physiological cascade between changed plasma hormone levels and hunger, satiation, or another parameter of eating. In a fully coupled endocrine control of eating, both links are coupled; in an uncoupled endocrine control, one or both links is uncoupled. As explained in the text, CCK satiation is apparently fully coupled, whereas leptin satiation and ghrelin secretion appear uncoupled.
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Fig. 5. Circadian rhythms of (top panel) serum leptin concentration (expressed as percent change from the 0800-h fasting level of 12.0±4.4 ng/ml), (middle panel) insulin (μU/ml), and (bottom panel) glucose (mg/dl). Note that meals, indicated by arrows in the x axis of the bottom panel, clearly affect insulin and glucose concentrations but do not affect leptin concentration. Data are from normal-weight men and women. The leptin pattern shown was similar in obese participants (BMI 38.8±2.5 kg/m2), but the 0800-h leptin level was significantly elevated (41.7±9.0 ng/ml). From Ref. [76], used with permission.
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Fig. 6. Linear relationships between plasma leptin concentration (ng/ml) and body fat mass (kg, measured by hydrodensitometry) in men (aged 19–41 years) and premenopausal (aged 19–45 years) and postmenopausal women (aged 49–87 years). Regression coefficients were .99, .95, and .92 in the three groups, respectively (all Ps<.0001). From Ref. [74], used with permission.
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Fig. 7. Intracerebroventricular injection of rabbit antimouse leptin antibodies increases food intake in rats. Filled symbols are cumulative food intake after injection with 10 μl preimmune IgG, and open symbols are cumulative food intakes following injection of 10 μl antileptin IgG (mean±S.E.M.). This dose of leptin antibodies has an in vitro binding capacity of about 1 ng rat leptin. The number of rats tested in each condition is represented by n. *Significant difference. From Ref. [15], used with permission.
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Fig. 8. Circadian rhythms of plasma ghrelin (pg/ml) in men and women who were either normal weight (BMI 27.3±0.9 kg/m2) or similarly obese who had lost weight either by dieting (matched obese controls; present BMI 40.0±3.9 kg/m2, initial BMI 48.2±5.2 kg/m2) or after gastric bypass surgery (present BMI 43.5±6.0 kg/m2, initial BMI 68.0±7.8 mg/m2). Note that (1) ghrelin levels increase progressively prior to meals and decrease after meals, (2) ghrelin also increases during the evening before decreasing during the early morning hours, and (3) ghrelin levels are greater in normal-weight than in obese participants. From Ref. [19], used with permission.
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Fig. 9. Surgical abdominal vagotomy (top panel) and abdominal deafferentation by perivagal capsaicin injection (bottom panel) each block the stimulatory effect on eating of intravenously infused ghrelin in rats. Controls are intact rats; open bars are saline injections; filled bars are ghrelin injections. These vagal lesions had no effect on the stimulatory effect of intracerebroventriculalry administered ghrelin (data not shown). *Significant difference. From Ref. [20], used with permission.
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Fig. 10. Intracerebroventricular injection of rabbit antirat ghrelin antibodies decreases food intake in rats. Open bars are food intake after injection with 10 μl preimmune IgG, and closed bars are intakes following injection of 10 μl antighrelin IgG (mean±S.E.M.). Top panel: 2-h food intakes in rats tested after an 8-h fast. Bottom panel: 12-h dark-phase food intakes in free-feeding rats injected at the beginning of the dark. *Significant decrease in food intake, P<.005, **P<.0001. From Ref. [65], used with permission.

My question is, if we are going to follow the "rules" of this book for instance, then do we still need MFP? I mean, do we still need to log and/or keep within a certain calorie a day?

My question is, if we are going to follow the "rules" of this book for instance, then do we still need MFP? I mean, do we still need to log and/or keep within a certain calorie a day?

I don't plan on counting/logging forever, MFP is a transition zone :happy: