| 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:
| • |
Types of sugar |
| • |
Amount
of sugars |
| • |
Brix levels of sweeteners |
| • |
Sweet-taste
perception in the mouth (Cephalic Response) |
| • |
Types
of artificial sweeteners |
| • |
-0-
Calories/Carbs |
| • |
Glycemic
Response |
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.
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