SWEET INFUSED FRUITS ™ (4 Patents-Pending) are produced by harvesting superior grade fruits and drying them to moisture specification. The fruit is then infused with a natural-sweet solution until a specific equilibrate Brix range is reached. Sweet Infused Fruits ™ processing involves a proprietary process, including distillation, extraction of high glycemic components, drying to juice powder stage, and sweet-infusion. The process conforms to all provisions of the Food, Drug, & Cosmetic Act.

The finished product is Certified Low Glycemic, and is ready to be added to snack foods, beverages, ice cream, chocolate, candy, or any other food as a sweet-flavor base. Nutraceuticals and Pharmaceutical preparations: Diet and Diabetic-Friendly formulas.

COUNTRY OF ORIGIN: USA

DESCRIPTION:
A light, free-flowing granular sweet fruit concentrate which can be used in place of high
glycemic sugars, sweeteners, and/or carbohydrates, and chemical sweeteners.

HISTORY OF USE: On the market, and broadly used in humans, since 1997.

MANUFACTURER:
Sweet Infused Fruits ™ Division
Nutrilab Corporation
St. Petersburg, FL.
www.SweetInfusedFruits.com
www. AcaiSweet.com
www. NutrilabUSA.com

REGULATORY STATUS: Sweet Fruit Concentrate, GRAS SINCE 1997

MANDATORY LABELING: All products containing Sweet Infused Fruits ™ shall bear the following information: Name of product: Sweet Infused Fruits ™, with the Ingredients as exactly stated herein.

INGREDIENT STATEMENT: Sweet Infused Fruits ™ (Fruit juice concentrate with Fruit Sugars, Acai fruit concentrate, Natural Kiwi Flavor with Other Natural Flavors, Silicon Dioxide [anti-caking agent]).

ALLERGIN STATEMENT: Sweet Infused Fruits ™ do not contain soy, egg products, milk products, peanuts, nuts, tree nuts (such as coconut), wheat or gluten, or seafood (including fish, Mollusks, or Crustacean).

BIOTERRORISM ACT: Our policy is to fully comply with the United States Bioterrorism Act, and to provide the government with any documents necessary to maintain the protection of the U.S.

U.S. RAW MATERIALS: Sweet Infused Fruits ™ do not contain any ingredient that does not originate from within the borders of the United States of America. As such, we do not purchase any ingredients from China, or any other foreign entity.

STORAGE RECOMMENDATIONS: This product is hygroscopic and must be kept sealed in a dry, humidity controlled atmosphere. Recommended shipping and storage of 50 degrees to 70 degrees F (10 degrees – 21 degrees C), 50% relative humidity. Protect from moisture and heat. Cold storage is acceptable. Do not freeze. Refrigeration acceptable.

EXPECTED SHELF-LIFE: 24 months @ < 75 degrees F, no humidity exposure, 3 years under Storage Recommendations conditions.

MSDS: Available upon request

www.SkinnyScience.com
www.SkinnyScienceEDU.com

Recently, Sweet Infused Fruits ™ were selected to provide the base of a new breed of Low Glycemic foods called Skinny Science ®.

Researchers for Skinny Science ® analyzed hundreds of potential sweeteners and raw materials for inclusion in their Low Glycemic foods line, and ended up choosing Sweet Infused Fruits ™, due to their anti-carbohydrate, Low Glycemic, and Non-Cephalic properties.

Skinny Science ® researchers have been working on weight control, obesity, and diabetes for three decades and have recently completed the design of their Low Glycemic line of Skinny Science ® products, including coffee, creamer, Acia Sweet ™ (a Low Glycemic Fruit Sweetener), and other products which contain Sweet Infused Fruits ™.

Board Approved Human In Vivo Clinical Trials have been conducted on the Skinny Science ® foods. The trials proved that the Sweet Infused Fruits ™ products are Low Glycemic and do not trigger LPL human adipose tissue fat-storage.

KID FRIENDLY
Skinny Science ® researchers are introducing a new line of Kid Friendly products that meet the strict protocol of the Glycemic Research Institute (GRI) Kid-Friendly Certification Program. The Kid-Friendly prococol is the strictest in the industry, and foods meeting the guidelines must comply with a plethora of standards all directed at protecting children from unsafe ingredients, and ingredients that exacerbate obesity and diabetes. The protocol may be seen at: www.GRIKidFriendly.com

The Cephalic Fat Spiral

2007

So, the brain has a conditioned response in reaction to eating something sweet.

It is called the Cephalic Phase Insulin Response (CPIR), and it’s responsible for the fat-storing effects of diet beverages, including diet sodas, diet tea, coffee, energy drinks, sports drinks, and flavored waters.

This adaptation in humans is a reaction to the ingestion of sweet-tasting foods. The body learned to associate sweet-taste on the tongue with the resulting sugar-energy-load that landed in the stomach.

The brain came to perceive sweet-taste with the need to program the liver to
prepare for the arrival of an outside source of high energy – sugar.

As the tongue senses something sweet, it programs the brain to set into motion a series of biochemical events. It doesn’t matter if the sweet taste comes from natural honey or from artificial sweeteners.

This biochemical cascade triggers the liver to stop the manufacture of protein and starch from its body-reserves, and to begin to store the glucose-energy that circulates in the blood.

In the case of diet beverages, the sweet taste sets these events into motion.

But when no calories actually appear in the stomach, this causes the body to demand real food, with resulting hyper-urges from the liver to overeat, or to drink more of the sweet-tasting liquid, and the cascade repeats itself.

Almost instantly, the body starts producing insulin, the “fat” hormone, which stores sugar in the blood stream, and programs the adipose tissue fat cells (belly fat) to store, store, store.

This Cephalic Phase Insulin Response (CPIR) creates reactive hypoglycemia (low blood sugar), which further triggers strong cravings for more sweet-tasting items, and high glycemic foods.

After the taste buds are activated by a sweet-taste, the urge to ingest food can last from 1 to 2 hours. So, you are hungry for hours, because no real food or calories has satiated the body’s need for energy.

And now, the body is producing insulin for no reason, because the brain has instructed the liver to store instead of burn/release its storage supplies.

The result is fat, fat, fatter - the Cephalic Fat Spiral.

Independent Research Document
Glycemic Research Institute

www.Glycemic.com
www.CephalicResearch.com

2007-2008

State-of-the-Art biomedical research has identified the key factors related to obesity, weight management, insulin resistance, and type 2 diabetes in humans. The primary factors are:

EVOLUTIONARY INFLUENCES

Obesity is obviously a consequence of increased food intake, driven by palatability and marketing, while the over-riding endocrine and genetic factors are silent partners in the obesity epidemic.

Anthropological-driven hormonal factors, such as Serotonin and Testosterone, stimulate humans to “eat all the time" and in great variety, thus persons genetically destined to become obese may eat more often, more rapidly, and in larger quantity before reaching satiety.

The role of hard-wired food-related mechanisms are currently being explored, such as Agouti-related protein (AgRP), a hypothalamic peptide involved in the regulation of feeding.

ADIPOSE FAT-STIMULATION VIA SWEETENERS

One of the major evolutionary tricks for survival is the desire for fattening foods. Without sufficient body fat levels in the female, the human species cannot procreate, and becomes extinct. This is observed in anorexics, in which low body fat results in cessation of menses and thus the inability to produce children. In males, low body fat levels do not prevent procreation.

Ergo, the female of the human species is hard-wired to create and hold higher body fat levels. In terms of survival of the species, the fatter, the better.

This is not a preferable advantage in a society of abundant and fattening foods. But, the brain is unaware of this fact, and cannot fathom that there are grocery stores and fast food. It could take hundreds of years before humans evolve to the point that the brain understands that there is food-a-plenty.

SWEETENERS THAT TAKE ADVANTAGE OF ANTHROPOLOGY

Sweeteners, both natural and synthetic, can stimulate adipose tissue fat-storage, primarily in belly-fat. In the female, procreation requires adequate levels of adipose tissue abdominal fat (belly fat). This area-specific fat helps insure a healthy baby.

The biochemical mechanisms that separate natural and synthetic sweeteners vary, but the result is the same, weight gain, more and larger fat cells, insulin resistance, and increase in incidence of type 2 diabetes.

Natural sweeteners can cause fat-cell-stimulation as can artificial sweeteners. Neither are exempt from contributing to human obesity and diabetes.

Sweeteners that contain -0- sugars, -0- fat, and -0- carbohydrates can still trigger abdominal obesity (belly fat) and parallel increases in type 2 diabetes and insulin resistance.

The culprits, in both natural and artificial sweeteners, can be identified as:

In foods and beverages, some sweeteners are not labeled as sugars, but act like sugars, such as Maltodextrins. Though the food/beverage label may state -0- sugars, there may be enough non-labeled sugars to cause huge elevations in blood glucose, insulin, Cephalic, and LPL fat-storage.

Foods, snacks, and beverages that contain fat-storing sweeteners, such as sugar (sucrose) and/or glucose, leads to dopaminergic and endorphin brain reward signals, with gastrointestinal satiety mechanisms leading to negative feedback from the gut via hormonal output.

PROTOCOLS

The effects of sweet taste and energy content on fat-stimulating responses can be quantified in Human In Vivo clinical trials. This requires the implementation of specific protocols that have been designed to measure the concomitant changes in blood glucose, insulin concentrations, and other perimeters, as related to oral ingestion of various sugars and sweeteners.

In the natural sugars and carbohydrates arena, sucrose, glucose, and maltodextrins are the most commonly used ingredient in foods and beverages.

Identifying fat-storing perimeters in artificial sweeteners is more complicated, and requires Cephalic testing. Combinations of natural sugars and artificial sweeteners mandates bi-and tri-level clinical trials in humans designed to track known fat-storage mechanisms and bio-markers.

Current protocols in quantifying fat-storage mechanisms in humans include glycemic indexing, Cephalic testing, randomized crossover design trial with functional magnetic resonance imaging, gastric lipase secretion, changes in gastrointestinal transit activity, pancreatic exocrine response, and gut hormonal response.

In studies with six different olfactory stimuli, the medial orbitofrontal cortex represents pleasant taste experiences, while the lateral orbitofrontal cortex represents unpleasant taste stimuli. Specific portions of the brain build associations between different food-related stimuli.

In the design of food and beverages, manufacturers have addressed more than visual aspects. Taste, sweetness, olfactory, and cognitive inputs have been intensively used to advantage by food manufacturers, thus overriding evolutionarily developed satiety signals.

During clinical trials, quantification of fat-storage factors related to a specific sugar, or combination of sugars and sweeteners (1), can be accurately determined utilizing controls against a specific percent of sugar or carbohydrate solution dissolved in water (Test Agent).

If the sugar/sweetener is present in a food or beverage, Comparative Analysis Trials can used to compare the biochemical value of a sugar/sweetener with a control that does not contain any sugars or sweeteners (1).

Cephalic testing (CPIR) requires highly sophisticated methodologies and equipment designed to track brain-insulin-signaling with miniscule half-lives (1).

IDENTIFYING BIOCHEMICAL CULPRITS

Prolonged and significant signal decrease in the upper hypothalamus (P < 0.05) can be observed in whereas control agent will exhibit no such effect.

Ingested Test Agents that increase glycemic perimeters, blood glucose and/or insulin concentrations, and/or trigger an early rise in insulin concentrations and/or Cephalic Phase Insulin Response (CPIR) are considered culprits in weight gain, obesity, type 2 diabetes, and insulin resistance.

PATHOLOGY of SUCROSE & GLUCOSE FAT-STORAGE

Aside from stimulating glycemic and insulinogenic perimeters, high glycemic sugars such as sucrose and glucose, can stimulate intense fat-storage, reactive hypoglycemia, as well as Cephalic Response via the brain.

There is a prolonged dose-dependent decrease in the blood oxygen level dependent (BOLD) magnetic resonance imaging (MRI) signal in the hypothalamus a few minutes after the ingestion of a glucose solution.

BOLD functional MRI (fMRI) measures changes in neuronal activity levels based on the associated changes in the local concentrations of oxygenated and deoxygenated hemoglobin.

Hypothalamic response to sweet taste and energy content of the sucrose/glucose mix and concomitant changes in blood glucose and insulin concentrations: Sucrose/glucose ingestion resulted in a prolonged signal decrease in the upper hypothalamus, with a negative early rise in plasma insulin.

Parallel observations have been identified in which researchers found a preeminent role of glucose in triggering cephalic phase insulin release (CPIR). Early decrease in the hypothalamic signal, is observed post-glucose ingestion, and is associated with CPIR.

Further, glucose is associated with an early rise in insulin concentration, and glucose triggers a decrease in fMRI signal in the upper hypothalamus. The additional decrease in fMRI signal is associated with a rise in insulin concentration.

DIABETIC INSULIN PROFILES

Use of sucrose/glucose mixtures and or glucose without sucrose, leads to a diabetic insulin profile as associated with a higher glucose peak and a prolonged duration of hyperglycemia.

Insulin secretion can occur in a biphasic manner depending on the type and magnitude of the glucose stimulus (dose/level). Chronic hyperinsulinemia can lead to -cell exhaustion, causing down-regulation of the insulin receptor and increasing insulin resistance, which can produce negative consequences on the vascular endothelium.

The magnitude of the first phase of CPIR occurs in response to a single-step glucose stimulus increases with increasing doses of glucose. The amount of insulin released during this phase is a sigmoidal function of glucose concentration (with a half-maximum for glucose of 135 mg/dl). If ingestion continues in short intervals, this first-phase insulin response is inhibited; in contrast, if longer time intervals are used, enhancement of the first-phase insulin response is observed at the second stimulation.

BIPHASIC INSULIN RESPONSE

First phase of CPIR occurs instantaneously after ingestion of a Cephalic agent, while the 2nd CPIR phase can last for a few hours, if the -cell is continuously exposed to glucose.

Source: Glycemic Research Institute/Cephalic Research Institute

DEFINING LIPOGENESIS (FAT-STORAGE)

Lipogenesis is the process that converts excess dietary carbohydrates into fat for storage as a source of long-term energy (adipogenesis). The deposition of fat and/or the conversion of carbohydrate or protein to fat, in this case facilitated by sucrose/glucose ingestion, changes insulin concentrations post-prandially, and correlates positively with a change in hepatic lipogenesis resulting in adipose tissue fat-storage.
.
IN CONCLUSION

Foods and beverages with zero sugars and zero calories can trigger fat-storage and insulin release. Swallowing the food or beverage is obsolete to the Cephalic Response.

Cephalic phase hormonal release occurs through activation of vagal-efferent fibers in response to food-related sensory stimuli. Tasting, chewing and expectorating food elicits hormonal release prior to nutrient absorption.

With properly designed clinical trials, the physiological consequences of ingesting various sugars, carbohydrates, and sweeteners can be identified and quantified.

The resulting data is an educational tool for the public fighting an obesity and diabetic epidemic, as well as a metabolic map for food and beverage manufacturers.