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BBS (Body Building Supplements)

Feel Full

Feel Full

FEEL FULL Is the first of its kind – 100% natural-hormone appetite control! Boosts CCK so you feel full!

  • Bypass “Get Fat” Ice Age Genes
  • Stimulant-Free—NO EPHEDRA
  • Lower Insulin, reduce craving
  • With BINGEBLOCKER, Combats N.E.S. (Night Eating Syndrome)
  • With LEANGUARD, Lose Fat, keep lean sexy muscle
  • Suppresses Stress Hormones like Cortisol

Using Your Own Hormones to Lose Fat, Preserve Muscle

FEEL FULL is the first formula to harnesses the power of the body's own feel full hormone (CCK) to reduce hunger. FEEL FULL also suppresses catabolic cortisol. FEEL FULL "tricks" the body into thinking it has eaten enough, creating the hormonal profile of the lucky few genetically lean.

CCK is a powerful internal hormone. After eating, CCK levels rise signaling the brain to stop eating. However, up to 20% of the population has deranged CCK. As a holdover of caveman times when constant hunger helped survival, these individuals' CCK does not rise enough, or they lack CCK receptor sensitivity.

FEEL FULL contains nutrients medically proven to raise CCK levels. Glycomacropeptides, phenylalanine, phosphatidylcholine and plant extracts boost CCK levels quickly and predictably. FEEL FULL reduces hunger, giving you hormonal willpower when you need it.

FEEL FULL solves another fat loss roadblock-cortisol. Eating less results in cortisol spikes, creating stressful feelings and binging. FEEL FULL's phosphatidylserine and glutamine peptides, both shown to blunt cortisol, also help protect hard-earned muscle from cortisol induced catabolism.

FEEL FULL is taken prior to "at risk" periods--times when you're tempted to overeat or binge. This time is customized to each individual. For some, at risk may be late at night. For others, perhaps mid-afternoon. Whenever you FEEL FULL, appetite is curbed, and you'll feel fuller and more in control.

Caveman genes may be the cause of CCK overeating, but it's also the solution. FEEL FULL harnesses the power of your own CCK, while defeating stress hormones.


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Carbohydrate Blocker Diet and Weight Loss Low Carbohydrate

Frequently Asked Questions about Feel Full™

Q: How do I take FEEL FULL?

A: Swallow 1-3 tablets 30 minutes before a meal or “at risk” period.

Q: How does it work?

A: It naturally and safely boosts your “feel full hormone” so you eat less.

Q: How long does it last?

A: FEEL FULL reduces appetite for about two hours; plenty to dodge the bullet of cravings and binging at night. Fight N.E.S. (Night Eating Syndrome)

Q: What other benefits does it produce?

A: Also normalizes blood sugar and insulin; helps you burn your own fat for energy; assists in lowering cholesterol and blood fats. Improves mood. New obesity research shows virtually every heavy person has elevated stress hormone (cortisol) levels.


HARNESS YOUR "FEEL FULL" HORMONE FOR FAT LOSS

By Bob Fritz

Open any health magazine and you see exciting medical advances about getting lean by adjusting your own hormones. Exotic names like leptin are thrown about, with the promise of a pill that can help you get—and stay—lean and trim. Indeed, it seems inevitable that these and other newly discovered hormones will be part of future weight control. But at the end of every story that starts out with such soaring fat loss expectations, the last sentence is the same: it will be years before these skinny pills become available.

But you don’t have to wait years for a “lean hormone” solution. There is an overlooked, yet powerful hormone inside your body that deserves closer attention. In fact, this hormone may actually rival the new fat loss discoveries. This hormone helps you “feel full” so you eat up to 30% less.

But first, why it is so hard to get lean in the first place, and how can this hormone help you eat less. The answers to both are rooted in our caveman genes.

Your Inner Caveman

You have an inner caveman; his genes live in you today. As a holdover from the last Ice Age, this caveman evolved to get and stay fat. Fat insulates from the cold and helps store energy when another meal does not come around for awhile. We are the descendents of cavemen whose bodies were designed to get as fat—and stay as fat—as possible. Those cavemen lived, those with wimpy appetites died.

One way to get and stay fat was to be constantly hungry. There were no anorexic cavemen who shoved away from a meal and declared eating any more would ruin his waistline. No, he evolved to gorge on almost any food whenever and wherever possible.

Early humans evolved a powerful set of metabolic tricks to help keep us fat and hungry today. These tricks were built in over 5 million years of brutal, grinding existence that favored guys who got and stayed fat. This is the battle: your inner caveman’s 5 million year old hardwired evolutionary fat genes against your puny desires to get lean. Guess who wins?

For example, when you cut calories—even a little—your body panics and thinks starvation. Alarm bells are sounded and almost immediately, your body slows its metabolic rate. Which means you burn fewer calories and stay fat. Talk about a mismatch. You eat less to lose fat, while your inner caveman body slows down to hang on to that fat. And the more you cut calories, the slower your body metabolism goes.

Similarly, missing a meal-or even being late for a meal-triggers the caveman inside into starvation mode again. Stress hormones like cortisol rise, causing a breakdown of tissue, including muscle. Losing lean muscle slows metabolism and breaks down the very muscle tissue that burns calories in the first place. Like I said, it’s an unfair mismatch.

The body has many other tricks, of course. Today, you crave foods that were scarce in caveman days: sugar, fat, protein and salt. As in jerky, ice cream, cake and other fast food. We crave these foods today because cavemen found these rarely, and so evolved cravings to constantly search for them.

Sounds depressing. We’re seemingly doomed to a lifetime of our inner caveman raiding the refrigerator at midnight, or craving donuts with the obsession of a heroin addict. Is our fatness scripted before we’re born?

Now for the good news. There is mounting evidence that harnessing our own “feel full” hormone can actually overcome these caveman urges. Basically, you “trick” your body into not being hungry. Better yet, natural supplements are the key to achieving this benefit.

CCK, The “Feel Full” Hormone

Back to that hormone that prompts you to eat less. This hormone is a mouthful called cholecystokinin-CCK for short. CCK has been studied for decades and is known as a powerful “feel full” hormone. When you eat food, especially proteins and fats, CCK is produced, mostly in the intestine. This elevated CCK reaches your brain and signals the body to stop eating.

Problem is, a surprisingly large percentage of today’s cavemen have a “deranged” CCK metabolism. In these individuals, CCK does not properly signal satiety (fullness). This survival holdover translates into virtual 24/7 hunger. Science knows that in some, CCK may not rise sufficiently to signal satiety, while others do not seem to have receptors that recognize CCK signals. Whatever the cause, faulty CCK metabolism kept cavemen—and you today—in constant hunger.

25 years ago, doctors learned that raising CCK levels through taking CCK itself raised levels. These elevated CCK levels resulted in reduced hunger and weight loss. More recently, medical studies have revealed the power of certain natural food supplements to also raise CCK levels. These nutrients can be taken at specific times to help block binge eating.

Blocking the Binge

Binge, gorge, pigout. All names for overeating. This stuffing behavior is a relic from cavemen at a kill. People with CCK issues have times when their caveman genes scream stuff yourself-now!

The time at which CCK runs low and signals the body to binge is highly individual. For some, it’s night time eating. A bright guy once observed that if everybody went to sleep at 8 at night, there would be no fat people. For others, the “at risk” period may be at dinner with friends with nachos in front of you. While those with normal CCK push away from the table after a meal, you might eat the tablecloth when in this state.

These nutrients are taken prior to your individual at risk period. CCK levels can be spiked prior to this at-risk period so you’re less hungry when you would normally be starving. Your inner caveman says, “I’m not so hungry, so call off the starvation dogs and eat less this--time.”

How much less do you eat with elevated CCK? Medical studies point to a reduction of an impressive 10-30% less food eaten. This reduction at a single meal may not appear impressive. However, on an ongoing basis this translates into a healthy 2-4 lbs of fat loss per month. Lean, ripped, sexy muscle—there all along—will now be revealed. You have achieved the rare metabolism of the genetically lean person who does not overeat. You have turned some of the body’s fat tricks in your favor, all without the use of drugs.

CCK Management Plan

Listed below are natural nutrients demonstrated to boost CCK, leading to reduced appetite. In turn, eating less results in weight loss. These nutrients run the gamit of exotic peptides to rare plants to familiar amino acids. Virtually all are available at health food stores, while others are somewhat new and may take some searching. However, all have been studied and are considered quite effective.

L-Phenylalanine. This versatile amino acid performs a number of functions that help natural bodybuilders, among them increasing CCK. L-Phenylalanine also boosts neurotransmitter production to help sharpen mental focus and acuity. Glycomacropeptide. This peptide is derived from milk and been shown to also increase CCK levels. It also appears to help lower blood pressure, among other benefits. Glycomacropepties are almost drug-like in power, and are an exciting addition to natural nutrition.

PC (phosphatidylcholine) This phospholipid has recently been discovered to increase CCK, reducing appetite. PC is derived from soy and is also indicated to boost mental function. PC is also involved in certain types of growth hormone increases.

Kidney bean (Phaseolus vulgaris) increases CCK, which reduces appetite. It also serves as an effective “starch blocker” helping to reduce the excess glycemic effects of carbohydrate intake.

Salaretin (Salacia reticulate) is a relatively new plant-based starch blocker that also normalizes blood sugar and insulin levels.

There are other natural nutrients that can help the CCK feel full strategy. For example, glutamine peptides can protect lean muscle from muscle loss that occurs during dieting. As mentioned, when you eat less, muscle is typically lost which slows metabolism. Protecting lean muscle helps you continue to burn fat.

Phosphatidylserine from soy lipids can blunt cortisol spikes, which helps reverse muscle breakdown even further. Additionally, elevated cortisol levels are strongly associated with virtually every eating disorder, especially binging. So naturally lowering cortisol with PS helps with both the mental and physical aspects of fat loss.

Take these nutrients 30 minutes prior to a meal, or before your personal at risk period. Within this half hour, CCK will rise signaling you not to eat as much. Simple and do-able in the real world.

While leptin and other exotic hormones are years off, the ability to curb hunger using your own CCK hormone is here today. As a side benefit, harnessing CCK is cost effective because you save on the food you don’t eat. But best of all, this effective strategy is 100% natural and can be used for pre contest preparation to shed a few pounds, or year round to remain lean.


Clinical Studies of Feel Full™


Relationship of satiety to postprandial glycaemic, insulin and cholecystokinin responses.

Holt S, Brand J, Soveny C, Hansky J


Department of Biochemistry, University of Sydney, Melbourne, Australia.

The effect of plasma glucose on satiety and the capacity of carbohydrates to stimulate cholecystokinin (CCK) remain unclear. The aim of this study was to test the hypothesis that the magnitude of the postprandial plasma glucose and insulin response is inversely related to the CCK response and to subjective satiety. Seven healthy, male volunteers consumed equal carbohydrate portions (0.5 g/kg body weight) of six test meals (Rice Bubbles, Sustain, Vita-Brits, All-Bran, porridge and white bread) in random order after an overnight fast. An egg and bacon meal was consumed as a non-carbohydrate control providing 0.5 g protein/kg body weight. Serum CCK, plasma glucose and insulin and subjective satiety (measured by a rating scale) were assessed over 3 h and quantified using the glycaemic index (GI), insulin index (II), the peak satiety score and area under the incremental curve (AUC). The observed GIs (mean +/- SE) ranged from 42.5 +/- 2.6 for All-Bran to 116.2 +/- 11.4 for Rice Bubbles, using white bread as the reference food (GI = 100). Peak satiety scores varied eightfold from 0.21 +/- 0.4 for Sustain to 1.64 +/- 0.4 for All-Bran. Significant inverse relationships were observed between the peak satiety score and both the glycaemic and insulin index of the seven meals (r = -0.916, p less than 0.001 and r = -0.926, p less than 0.001). A direct relationship was observed between satiety (AUC) and the CCK response (AUC) (r = 0.73 p less than 0.01). The results suggest that glycaemic and insulin responses to carbohydrate foods are inversely proportional to the CCK response and satiety.


The addition of soybean phosphatidylcholine to triglyceride increases suppressive effects on food intake and gastric emptying in rats.

Nishimukai M, Hara H, Aoyama Y.

Division of Applied Bioscience, Graduate School of Agriculture, Hokkaido University, Sapporo 060-8589, Japan.

The physiologic roles of dietary lecithin have not yet been clearly defined. We examined the effects of soybean lecithin on gastric emptying (Experiments 1 and 2) and food intake (Experiment 3) in rats. Male Wistar rats were fed 2 g of a 20 g lipid/100 g diet containing various levels of lecithin after 24 h of food deprivation; gastric contents were collected 3 h after feeding (Experiment 1). In Experiment 2, the effects of lecithin and a CCK-A receptor antagonist on gastric emptying were examined using a modified phenol red recovery technique. In Experiment 3, their effects on food intake were examined after an intraduodenal infusion of an oil emulsion containing 50 mg soybean oil (SO) or SO partially replaced by lecithin (14-50%). Gastric emptying rates of the lipid and protein in the test diet (Experiment 1) or of phenol red (Experiment 2) were lower in the groups administered lecithin. Food intake for 60 min was lower in rats infused with the oil emulsion containing lecithin (25, 50%) than in rats not administered lecithin. The suppressive effects of lecithin on gastric emptying and food intake were largely reduced by devazepide. These results demonstrate that oil containing lecithin inhibits gastric emptying and food intake, and the effects are associated in part with CCK release.


Cholecystokinin-A Receptors Are Involved in Food Intake Suppression in Rats after Intake of all Fats and Carbohydrates Tested.

Bellissimo N, Anderson GH.

Department of Nutritional Sciences, Faculty of Medicine, UniversityofToronto,Toronto,ON,Canada M5S 3E2.

The hypothesis of these studies was that all fats and carbohydrates suppress food intake, at least in part, via cholecystokinin-A receptors (CCKAR). Fat (coconut oil, beef tallow, olive and safflower oil) and carbohydrate (cornstarch, sucrose, glucose and fructose) preloads were given intragastrically (1 g/4 mL) 30 min before feeding. Devazepide (0.25 mg/kg), a CCKAR antagonist, was given intraperitoneally at 60 or 30 min before or with each of the macronutrient preloads. Devazepide reversed food intake suppression caused by all fat and carbohydrate sources, but the effect was not consistently related to the time of devazepide administration or to any specific feeding interval. Among the fats, coconut and olive oil were most responsive to devazepide. The effect of all carbohydrates on food intake was decreased by devazepide. We conclude that CCKAR play a role in food intake suppression caused by all fats and carbohydrates, but their role is dependent upon the composition of the fat or carbohydrate.

PMID: 12840200 [PubMed - in process]


Predicting cardiovascular risk factors from plasma cortisol measured during oral glucose tolerance tests.

Reynolds RM, Syddall HE, Walker BR, Wood PJ, Phillips DI.

Medical Research Council Environmental Epidemiology Unit, University of Southampton, Southampton,UK.
Increasing evidence suggests that activation of the hypothalamic-pituitary-adrenal (HPA) axis may contribute to the pathogenesis of the metabolic syndrome and obesity. The mechanisms are unknown but may involve alterations in the metabolic responses to feeding that interact with the HPA axis. As it is known that plasma cortisol falls during an oral glucose tolerance test (OGTT), changes in cortisol measured during an OGTT may be altered in the metabolic syndrome. We measured changes in plasma cortisol during OGTTs in a large study of 593 men and women to determine correlates of changes in cortisol with features of the metabolic syndrome and the extent to which these relationships are confounded by obesity. In men and women, higher cortisol area under the curve (AUC) during the OGTT was associated with higher glucose AUC and higher systolic blood pressure. Higher cortisol AUC was associated with reduced insulin increment in men, but higher 2-hour insulin and insulin AUC in women. However, the decline in plasma cortisol after glucose administration was poorly predictive of features of the metabolic syndrome. Obesity was associated with lower cortisol AUC but not with percentage decline in cortisol. Plasma cortisol and obesity had independent effects on plasma glucose and were the strongest predictors of plasma glucose in multiple regression analysis. Measurements of plasma cortisol during the OGTT reinforce the previously observed relationships of activation of the HPA axis in the metabolic syndrome. However, the altered HPA response to feeding does not appear to be primarily responsible for HPA activation in subjects with the metabolic syndrome.

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