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Recommended
Readings:
Nutrient Density Explored
Introduction
Meals
Meals are the basic measurement for caloric
consumption due to the fact that the amount of food you consume is
determined by the size and frequency of your meals. Three basic phases
which affect your meals are hunger, satiation, and satiety. These aspects
will be broken down subsequently.
Dual Center Hypothesis
Hunger may be defined as the sensation which drives
an individual to find and consume food [1]. In 1940, Hetherington and
Ranson postulated that feeding involved activation of the lateral
hypothalamus (LHA). They found two areas of the hypothalamus that monitor
feeding and body fat [2]. Shortly thereafter, the dual center hypothesis
was invented [3]. This states that the LHA is responsible for hunger and
subsequent feeding, while the ventromedial hypothalamus (VMH)
is responsible for satiety and satiation. To clarify, after the ingestion
of a certain amount of food, a suppression of hunger occurs
that will lead to the termination of feeding. This is referred to as
satiation. The feeling of fullness between meals is referred to as
satiety [1].
Recent experiments have brought support to this
hypothesis. For instance, studies show electrical impulses on the lateral
hypothalamic area of animals results in feeding, while an impulse on the
ventromedial aspect promotes satiation and eventual termination of feeding
[4, 5, 6]. Moreover, it has been shown that harming the VMH leads to
insulin resistance and hyperinsulinemia in animals. Further, subjects with
an injured VMH eat an immense amount of excess calories, resulting in
obesity [7, 8].
While the roles of the lateral and ventromedial
hypothalamic areas are well established, the dual center hypothesis is
simplistic to say the least. You see, there are many more mechanisms which
control feeding and satiation. For instance, nuclei throughout the
inferior brain stem collaborate and deliver messages to endocrine organs
and forebrain structures. The midbrain and thalamus further interpret this
information in accordance to the sensory properties of food, and the
forebrain nuclei communicate the positive aspects of feeding.
These feeding centers are informed by multitudes of hormonal and neural
outputs on the metabolic stasis of the body [1, 9].
A variety of other factors such as insulin,
neuropeptide Y, leptin, catecholamines, and ghrelin must be taken into
account. Today we are going to discuss these factors and how you, the
athlete, can properly manipulate them to achieve your goals.
Feeding Regulation
A multitude of elements can influence your caloric
intake, but these can be simplified into two categories: anorexigenic and
orexigenic factors. The former promotes a lack or loss of appetite for
food, while the latter results in a desire for food. Some topics discussed
will be a combination of both. We begin with the protein hormone leptin.
Leptin
Leptin is a protein hormone secreted from adipose
tissue [10]. Since its discovery, leptin has been considered a contributor
to satiety [11]. Multitudes of studies confirm this hypothesis. For
instance, leptin reduced food consumption and body weight when
given to rats intraperitoneally (administered by entering the peritoneum,
which is the membrane that lines the cavity of the abdomen), intravenously
(through veins), or intracerebrally (in the cerebrum) [12, 13, 14, 15,
16]. Furthermore, Chapelot et al. demonstrated that plasma leptin
concentrations increase during spontaneous intermeal intervals, and
decline before the onset of a meal, showing leptin may contribute to meal
patterns [40].
Body fat is a huge factor in leptin concentrations.
The amount of leptin secreted into the blood stream is largely dictated by
how much fat one has. For example, leptin was measured in seventy-one
obese individuals and 108 normal weighted ones [17]. Leptin in the latter
group was measured at 8 ng/ml. Results showed the largest discrepancy
occurred when body fat reached over 25%—increasing anywhere from
three-tenfold.
Carbohydrates are also a potent leptin regulator.
Insulin given to rats increases leptin gene expression, and inhibits the
reduction in leptin mRNA caused by calorie restriction and fasting (i.e.
36 hours) [19, 20]. Similar effects have also been reported in humans [21,
22]. Glucose metabolism has been shown to be an important factor in leptin
utilization; this may be why insulin stimulates leptin secretion [42].
To add to the comment on calorie restriction, a
decrease of 10% in body weight has been shown to decrease leptin by 53% in
some cases [29]. Moreover, a decrease in leptin during starvation diets
will promote energy conservation by decreasing thyroid hormone-induced
thermogenesis (one way is by decreasing NPY, discussed later) and
increasing glucocorticoids that mobilize energy stores [1]. Brent et al.
tested the interactions between energy intake and fat loss on plasma
leptin during prolonged, moderate and severe energy restriction [43].
Mean leptin decreased markedly by up to 66% (P < 0.001) at week one of
energy restriction, and then gradually thereafter. Additionally, Keim,
Stern, and Havel tested the effect on women of a chronic energy deficit on
plasma leptin concentrations and self-reported appetite to explore
possible relations between leptin and appetite sensations [44]. Twelve
healthy women participated in a three-week study of neutral energy
balance, followed by 12 weeks of energy deficit (feeding reduced by 2 MJ/d
and energy expenditure increased by 0.8 MJ/d). Leptin
diminished by 54% after 1 week of a moderate energy deficit and remained
low after 6 and 12 weeks. Leptin was associated with self-reported hunger,
desire to eat, and prospective consumption; the largest increase in hunger
was associated with the sharpest decline in leptin. Moreover, leptin and
hunger were not influenced by the amount of weight and body fat lost.
Thus, fasting and very low-calorie diets lead to a decline in leptin
production.
Romon et al. sought out to test whether the
macronutrient content of the meal could influence postprandial (after
eating) leptin response, and if leptin levels were associated with
postprandial satiety, hunger, and subsequent food intake [31]. They used
22 healthy subjects (half male and half female) and had them eat a diet
consisting of carbohydrates (81%) or fat (79%), with about the same amount
of protein in each, while the third group fasted. In both genders, leptin
response was higher after the carbohydrate meal than after the fat meal or
while fasting. Leptin response was significantly correlated to insulin
response (r = 0.51, P < 0.0001). Leptin started to rapidly rise 4-5 hours
after a meal; however, leptin had no acute affect on hunger. This was
expected, though. Results show higher leptin concentrations results in
long-term satiety rather than short. For example, in rodents, food intake
was reduced after 4 hours of leptin administration [32]. While in monkeys,
leptin elicited its anorexic effects on the second day of injection [33].
An important mechanism by which leptin works is
inhibiting neuropeptide Y (NPY, which will be discussed in-depth further
on; just understand now that it is a major orexigenic peptide) synthesis
and release [23]. Cusin et al. demonstrated that injecting leptin in lean
rats diminished NPY synthesis in sites of production in the hypothalamus
[24]. Many other studies also testify to this [25, 26].
However, this clearly is not the only means by which
leptin works. Erickson, Clegg, and Palmiter demonstrated this by
injecting leptin into mutant mice deficient in NPY. Five days of leptin
administration significantly reduced their food intake, body weight, and
adipose tissue mass, showing that leptin can increase satiety by actions
independent of NPY [27].
Further research shows that glucocorticoids
negatively affect leptin. For instance, Zakrzewska et al. injected 3 µg of
leptin into three groups: normal rats, adrenalectomized rats (surgical
removal of an adrenal gland, this gland secretes glucocorticoids, the most
abundant in the body being cortisol), and adrenalectomized rats with the
added supplementation of glucocorticoids [28]. The first group showed a
small reduction in body weight and food consumption, the second group had
very strong and long-lasting reduction in food and body weight, while
supplementation with glucocorticoids in the third group inhibited leptin’s
effects. This may explain why people with Addison’s disease—a rare
endocrine disease that results from the underproduction of aldosterone and
cortisol by the adrenal glands—are usually hypophagic (under eat,
anorexic). Leptin may also exert its effects via the central nervous
system [41]. For more on glucocorticoids, refer to
Endocrine Insanity Part I
.
Leptin also acts synergistically with
choleocystokinin (CCK, discussed in-depth further on) to promote satiety
[35, 36, 37, 38]. To investigate the physiological relevance of this
observation, Julie et al. injected saline intraperitoneally (IP, near
abdominal organs) or CCK into 48-h-fasted or fed rats [39]. They
hypothesized that leptin deficiency, induced by fasting, weakened the
satiety response to CCK. Fasting blunted the satiety response to 3.0 µg/kg
of CCK, such that 30-min food intake was suppressed by 65.1% (relative to
saline-treated controls) in fasted rats vs. 85.9% in the fed state (P <
0.05). They also tested how NPY injections would affect CCK, and found
that this further attenuated its effects, further supporting the
hypothesis leptin deficiency, weakens the satiety response of CCK, as NPY
is higher when leptin is lower. There results were consistent with other
experiments that leptin does assist CCK.
A very fascinating study reported that leptin in
humans is secreted by circadian rhythms [30]. Madhur et al. tested the
24-h profiles of circulating leptin levels in three groups: obese, obese
people with non-insulin-dependent diabetes mellitus (NIDDM), and lean
individuals. In all the three groups, serum leptin levels were highest
between midnight and early morning hours, and lowest around noon to
midafternoon. They postulate that this inherit mechanism could be to
suppress appetite during the night when fasting. Now, while your night and
early morning leptin levels are higher, this can be manipulated according
to your diet. Havel, Townsend, and Teff portrayed that the mean daily
levels as well as the nocturnal (night) concentrations rise higher after
high-carbohydrate/low-fat meals than after low-carbohydrate/high-fat meals
[34]. For an in-depth analysis on the circadian rhythm, see Knowlden’s
(2002, 2003) sleeping articles in the anatomy section under ‘hormones’.
The study of leptin is quite fascinating. Look for a
full article on its many actions in the future. If you want to learn more
about leptin, refer to
Metabolic Primer Part II.
CCK
To introduce cholecystokinin (cho·le·cys·to·ki·nin,
CCK), here is a quote from King (2003) in ‘Endocrine Inanity Part 1’ [45]:
| Choleocystokinin is a peptide hormone
that originates in the duodenal mucosa endocrine cells. CCK is released in
the blood after an arrival of chyme (partly digested food) containing fat
or acid. CCK targets the gallbladder and the pancreatic acinar cells. Upon
the arrival of CCK, the gallbladder contracts, releasing its stored bile
into the duodenum. In the pancreas, CCK stimulates pancreatic enzymes
which are extremely important for the chemical digestion of various
foods in the small intestine. |
CCK is the most investigated satiety signal. In 1973,
Gibbs et al. gave purified or synthetic CCK to rats
before a meal and observed that it dose-dependently reduced the
size of the meal [48]. Since then, hundreds of experiments have
demonstrated CCK’s ability to reduce meal size, including in humans [48.
49, 50, 51]. Moreover, further evidence to this was given when many
scientists observed that injecting CCK-1 receptor antagonists
before a meal causes hyperphagia (over eating) in animals and humans [52,
53]. Additionally, older people commonly eat less than younger
individuals. To test what mechanism(s) produce(s) this anorexic effect,
MacIntosh et al. examined eight healthy, old (65–80 y) and seven young
(20–34 y) men after administrating lipids and glucose for 120 min on
separate days [78]. Plasma CCK, glucagon-like peptide 1 (GLP-1), and
peptide YY (PYY) concentrations were measured. CCK concentrations were
significantly higher in older than in younger subjects, while Plasma GLP-1
and PYY concentrations were not significantly different between groups.
A popular suggestion on how CCK works is that when
stimulated, it acts in a local paracrine manner to stimulate CCK1
receptors on the sensory fibers of the vagus, making the nerves sensitive
to CCK and other stimuli such as gastric distension, and further promotes
slow gastric emptying [55]. This is significant because stomach sensory
information is brought to the brain by these nerves, so making them more
sensitive would promote satiation. Results show that cutting vagus nerves
makes CCK worthless at reducing meal size, strongly supporting this
hypothesis [54]. Additionally, gastric distension is a potent signal in
satiety. For example, Geliebter, Westreich, and Gage inserted a balloon
into four lean and obese individuals [113]. They then filled the balloons
with 0-800 ml of water. The results showed that as volume increased, food
intake decreased.
Therefore, CCK relaxes the stomach and makes you very
sensitive to gastric pressure, promoting satiation [65]. Furthermore, CCK
stimulates pancreatic enzyme secretion [74], promotes gall bladder
contractions [75], constricts the pylorus [76], and by inhibiting gastric
emptying, promotes gastric distension [77].
CCK may also act as a neurotransmitter or
neuromodulator within the brain to inhibit gastric emptying. For example,
injection of CCK into the hypothalamic and nucleus of the solitary tract
have been observed to significantly inhibit gastric emptying [66, 67, 68].
Further, Roger et al. demonstrated that endogenous CCK may enter the
bloodstream to inhibit gastric emptying by an endocrine mechanism.
Moran McHugh tested for a mechanism by which CCK
promotes satiety [46]. They injected CCK into their participants and
tested for the rate of gastric emptying. Gastric emptying was inhibited by
this hormone. The onset of the inhibition is rapid, and its effect brief.
They concluded that CCK can be thought of as a link in a chain of
physiological elements—the satiety effect depends upon inhibition of
gastric emptying, which then leads to gastric distention with increased
food consumption. Additionally, CCK has a short half-life (1-2 minutes).
Because of this, injecting CCK 15 minutes before a meal is ineffective at
promoting satiation [56].
Scientists have studied extensively whether CCK would
be an effective supplement for reducing meal size in humans. The results
are disappointing. When CCK is given continuously, it quickly becomes
ineffective [58]. Moreover, when CCK is given before every meal in rats
for a short while, it is effective at reducing meal size, but the animals
compensate by eating more food over the next several days [57]. Thus far,
CCK does not appear to be an effective supplement, but rather must be
manipulated through diet. However, this also has its problems.
Studies show that humans adapt very quickly to high
fat diets (HFD), which subsequently decreases the satiating response to
nutrients. For instance, Cunningham et al. showed that consumption of a
high-fat diet for two weeks led to an acceleration in the gastric emptying
rate of high-fat test meals [59]. However, CCK is still raised very high
during HFD, making these results rather strange [60]. To test the
mechanisms by which this adaptation occurs, Covasa and Ritter injected CCK
into rats on low fat diets and high fat diets [61]. The former group had a
much slower rate of gastric emptying (26.2-55.1%) than the later group
(10.0-31.7%). This shows that HFD may cause subjects to be insensitive to
CCK’s satiating effects.
To further investigate this, French et al. had 12
male subjects consume a high-fat diet (58% energy) for two weeks, testing
levels of cholecystokinin (CCK), food intake, and subjective feelings of
hunger and fullness [62]. The results showed a significant enlargement in
the average daily food consumption, increasing feelings of hunger and
declining fullness. And again, CCK was substantially higher, further
supporting the hypothesis that high-fat diets reduce the body’s
sensitivity to this hormone.
Castiglione, Read, and French sought to test whether
this effect on gastric emptying was nutrient-specific [63]. Studies were
carried out on eight healthy, free-living male volunteers between the ages
of 19 and 26. Their original fat intake was between 30-40%. In the test
they increased this to 55% for 14 days. They then gave them high-fat and
high-carbohydrate meals. The high carbohydrate meals had nearly the same
rate of gastric emptying before and after the experiment. However, the
rate of lipid emptying was much faster, consistent with the previous
experiments. This shows HFD adaptations are nutrient-specific to fats, and
not to carbohydrates.
Now, most athletes never would have this much fat in
their diet. However, this does show the folly in excessively high-fat/low-carb
diets, which not surprisingly often advocate the wholly ignorant,
logically invalid, and completely unscientific protocol of fat and fiber
post-workout. Moreover, you can see that people who eat junk food
constantly (i.e. pizza) are going to be much more susceptible to continued
binges than someone on a lower fat diet. To exemplify the harm in this
adaptation, rats fed the same amount of fat at a slow rate consumed less
energy per day, had longer between-meal intervals, and gained
less weight over a two-week period than after infusion of fat
at a more rapid rate [125]. So, those reading need to take a close look at
their diet, and be sure they are not consuming excessive amounts of fat
right now.
As displayed above, the greatest stimulator of CCK is
fat [47]. Carbohydrates are very poor CCK producers, while proteins, on
the other hand, may be potent CCK manufacturers. For example, Forster and
Dockray gave rats a liquid test meal of peptone. The results showed
delayed gastric emptying and a short elevated response in CCK, lasting ten
min or less [69]. Further, Sharara et al. administrated proteins, protein
hydrolysates, amino acids, glucose, and starch to several subjects [70].
The results showed intact proteins were the only nutrients to stimulate
CCK release. It is postulated that protein stimulates CCK by reducing
trypsin degradation of CCK releasing factors in the intestinal lumen [71].
This is significant because administration of trypsin antagonists elevates
plasma CCK levels [72]. To test this hypothesis, Woltman and Reidelberger
composed a rather genius experiment [73]. Using non-fasted rats, they gave
peptone alone, and peptone with Devazepide, which is a CCK antagonist. If
CCK does assist proteins satiating effects, then devazepide should
significantly attenuate peptone-induced anorexia. The results showed
peptone by itself decreased food intake by 18-96%, while devazepide with
peptone decreased these effects by 29-65%. This strongly suggests that CCK
plays a major role in the satiety response to duodenal delivery of
protein.
Glucostatic Theory
Here is another quote from Joe King in,
Metabolic Primer Part II explaining the glucostatic theory.
According to the glucostatic
theory of food intake regulation, the satiety center neurons are sensitive
to blood glucose levels: high levels increase and low levels decrease
their activity. Low blood sugar reduces the inhibition of the feeding
center by the satiety center, resulting in hunger and feeding. After
absorption, increased blood sugar activates the satiety center, which will
inhibit the feeding center (this process works by negative feedback, which
was examined in Endocrine Insanity Part II). During ingestion, the
stimulation of gustatory and mechanical sensors in the mouth and the
distention of the stomach inhibit the feeding center.
In the 1950s, Jean Mayer composed various experiments
on rats and mice that lead to the glucostatic theory [87]. Studies In the
‘60s and ‘70s by Steffens et al. showed that glucose is low at the onset
of a meal, and rises at meal termination [88, 89]. And further experiments
have given great establishment to this theory.
The theory states that glucose is monitored by the
central nervous system [82]. Evidence shows that glucoreceptors and
glucosensitive neurons in the hypothalamus do indeed perform this task
[83]. For example, Himmi, Boyer, and Orsini simultaneously monitored blood
glucose level and forebrain unit activity in rats [84].They injected
glucose or phlorizin into them and observed transient fluctuations in
glycemia, occurring either spontaneously or after the injections. They
noted spiked frequencies of more than one-third of the neurons tested in
the lateral hypothalamic area in response to the fluctuations. Most of the
cells were activated during hypoglycemia and depressed during
hyperglycemia. They concluded that, “These neurons might mediate the
effects of a drop in blood glucose on either meal initiation or
neuroendocrine or autonomic events related to nutritional functions.”
Several studies have also shown that the onset of a
meal is preceded by low blood sugar. Sylvestre and Magnen monitored blood
glucose levels in free-feeding rats for several hours and found that there
was a 6 to 8% fall in blood sugar, starting 5-6 min prior to meal onset,
before every meal from day to night [85]. Furthermore, Campfield, Smith,
Rosenbaum, and Hirsch sought to test whether changes of hunger ratings in
humans were related to spontaneous changes in blood glucose concentration
[86]. In 83% of the subjects, both the perception and behavioral
expression of hunger were preceded by and correlated with brief, transient
declines in blood glucose (10% at 27 min). They also are performing an
ongoing study by injecting insulin into subjects (which is a hypoglycemic
producing hormone). Early results in five subjects showed that hunger
increased after insulin-induced transient declines in blood glucose, but
no change in hunger occurs when blood glucose concentration are stable.
With this in mind, several factors must be taken into
account. First, we must discuss insulin, which helps regulate blood
glucose. Studies demonstrate that it has both orexigenic and anorexic
effects.
Insulin has contradicting results. Some studies show
it can increase hunger in animals and humans [93, 94]. But this is likely
because of its hypoglycemic qualities. Others show it promotes satiety.
Brief and Davis examined the effect of chronic infusions of insulin in one
of three doses (5, 7.5 or 10 mU/day) on food and water intake in rats. All
groups treated with insulin decreased food intake during the day and
night, and 10 mU/day produced a significantly greater reduction in water
intake than each of the other solutions [79]. Similar results were also
found in baboons [80, 81]. Additionally, if insulin or leptin
levels are increased within the brain, animals eat less food
and lose weight; on the other hand, if the normal leptin or
insulin signals within the brain are reduced, animals overeat
and become obese [101]. Overall, if used properly, insulin acts as a major
anorexigenic hormone. Additionally, insulin augments the satiating effects
of CCK [143]. Lastly, one of its most potent actions is inhibition of NPY/AgRP
and stimulation of a-MSH/CART neurons [148]. This will be discussed
further on.
Having a high-GI carb such as glucose has also been
shown to have a greater short-term satiety than having a slow-burning carb
such as oatmeal. This will be explained later.
It is worthy to note that high blood sugar promotes
satiety. Studies show hyperglycemia slows gastric emptying [96], increases
proximal gastric compliance [97], attenuates gallbladder contraction [98],
and prolongs small intestinal transit time [99], among other things [100].
This would contribute to the above results.
The problem with having high-GI carbs (concerning
hunger) is that you will promote hyperglycemia, and high blood sugar
induces an elevated concentration of insulin. The trouble with having high
bursts of insulin is that it acts as a hypoglycemic hormone (one that
decreases blood sugar). As displayed above, hypoglycemia induces hunger.
So for short term satiety, having pure glucose, such as a post-workout
shake, will have a more potent short-term satiety compared to complex carb.
However, in the long run, you want normal blood glucose levels. How to
manipulate slow-and fast-burning carbs for bulking and cutting cycles will
be discussed further on under practical applications.
NPY
The most potent bodily orexigenic substance known to
man is Neuropeptide Y (NPY) [1]. NPY is a major brain peptide located in
the hypothalamic arcuate nucleus (ARC) that projects to the
paraventricular nuclei (PVN) and dorsomedial nuclei (DMH), and is
postulated to control energy balance by stimulating feeding and inhibiting
thermogenesis, especially under conditions of energy deficit [1].
NPY levels rise in almost every situation of hunger.
This includes fasting and hypoglycemia. For example, Vettor et al.
administrated NPY to normal rats for 7 days [103]. The result was a
sustained threefold increase in food intake and an increase in body weight
over 40 g.
In order to find out if central injection NPY would
alter brown fat thermogenesis and white fat lipoprotein lipase activity,
Billington et al. injected NPY into three groups of rats: 1) NPY (5
micrograms/injection) and ad libitum food; 2) NPY (5 micrograms/injection)
and food restricted to control intake; 3) saline injection and ad libitum
food [102]. The first group ate much more food than the latter two, and
there was an increase in white fat lipid storage and a decreases brown fat
thermogenesis in both NPY groups.
Now, as stated above, by acting in the brain, insulin suppresses food
intake, whereas NPY has the opposite effect. Fasting increases NPY levels,
while lowering insulin levels. Therefore, Schwartz et al. hypothesized
that the anorexic effect of insulin could result from an insulinogenic
inhibition of NPY gene transcription [104]. To test this, they injected
insulin into rats after they fasted for 48 hours. The results showed
insulin significantly suppresses the expression of mRNA for NPY in lean
rats, strongly supporting their hypothesis and showing that fasting
increases NPY synthesis dependent on low insulin levels.
In another experiment, Zarjevski et al. chronically administrated 10
micrograms of NPY per day to female rats [105]. This resulted in
hyperphagia, increased basal insulinemia, as well as liver and adipose
tissue lipogenic (fat-building) activity.
To further demonstrate NPY’s effects, Sainsbury et al. injected NPY into
normal rats for 6 days. This resulted in hyperphagia, increased body
weight gain, hyperinsulinemia, hypercorticosteronemia, and
hypertriglyceridemia (elevated triglyceride levels), compared to control
rats [106]. NPY infusion also resulted in an insulin-resistant state in
muscles and in a state of insulin hyperresponsiveness in white adipose
tissue, as assessed by the measurement of the in vivo (within a living
body) glucose utilization index of these tissues.
What is interesting to note is that the above
side-effects were entirely prevented when rats were adrenalectomized
(surgical removal of an adrenal gland, which secretes glucocorticoids, the
most abundant in the body being cortisol) before NPY administration. Also,
levels of mRNA for leptin were increased in white adipose tissue after 6
days of NPY infusion in normal rats (due to hyperphagia), and white
adipose tissue weight was also increased (also due to hyperphagia). They
concluded that, “intact adrenal glands, and probably circulating
corticosterone (a glucocorticoid), in particular, are necessary for the
establishment of most of the hormonal and metabolic effects induced by
chronic…infusion of NPY in normal rats.”
You should now further understand the importance of leptin in hunger
regulation. Leptin’s ability to suppress NPY is a powerful satiety weapon.
Further, you can see why people on low-carb diets are always hungry.
Without carbs to facilitate a steady flow of insulin, not to mention blood
sugar, the subjects that participate in this are bound to be hungry and
have a multitude of carbohydrate cravings.
Feed Back Loop
The feed back loop involves leptin, NPY, and insulin
in relation to satiety. First, fasting or strict dieting results in a
decrease in leptin. Low concentrations of leptin then result in an
increase in NPY synthesis, which promotes feeding. After feeding, if the
food contains carbohydrates, insulin rises, which subsequently decreases
NPY production, resulting in satiation and eventual termination of
feeding. Moreover, as stated above, insulin also increases leptin
secretion from adipose tissue, further promoting long-term satiety and
decreased NPY concentrations. [18].
Ghrelin
Ghrelin (named after Proto-Indo-European roots "ghre"
for grow and "relin" for release) is one of the few, if not the
only, signal(s) in the gastrointestinal tract (GI tract) that stimulates
hunger. It is a 28-amino acid peptide that rises during prolonged fasts
and promotes feeding [108]. Ghrelin is also produced in the brain, and
there is some evidence that ghrelin signals are carried by vagal
afferent nerves to the brain [111]. Additionally, ghrelin is a
strong growth hormone producer [112].
A logical hypothesis is that ghrelin may contribute
to the onset of a meal. To test this, David et al. monitored 10 healthy
subjects for 24 hours, taking samples of Ghrelin 38 times throughout the
day [107]. Plasma ghrelin increased nearly twofold before the onset of a
meal, and fell back to normal levels 1 hour afterward. These results bring
strong evidence to ghrelin’s physiological role in meal initiation for
humans.
Wren et al. investigated the effects of ghrelin (5.0
pmol/kg/min) or saline infusion on hunger and food intake in a randomized
double-blind cross-over study in nine healthy volunteers [109]. The
results showed a statistically significant increase in energy consumed by
the participants. Wren et al. again composed an experiment on ghrelin and
its orexigenic effects, this time on rats [110]. He injected ghrelin at
various concentrations to rats, and observed hyperphagia and subsequent
obesity in the tested rats.
Ghrelin partially exerts its effects by speeding
gastric emptying [111]. Additionally, in rodents injected with ghrelin,
there is an increase in NPY and AgRP mRNA expression [111].
This peptide is very new, however, and much research
still needs to be done. Nevertheless, ghrelin seems to be a key player in
hunger regulation.
Posture
This next section is quite novel, to say the least.
It appears that posture can have a profound effect on digestion. For
example, Theresa et al. composed an experiment to test posture and meal
structure on gastric emptying and satiety [114]. Nine women ingested
tomato soup and then immediately or 20 min later an egg sandwich, when
seated or when supine (lying on their backs). The results showed the
half-emptying rate of the sandwich was 32% longer and the emptying rate
after lag phase was almost 39% slower for the subjects who were supine
compared to those who were seated upright. In those who consumed the soup
immediately before the sandwich, the half-emptying time of the soup was
50% longer. In subjects who waited 20 minutes to consume the sandwich,
however, the after-eating satiety lasted a bit longer, but in those that
ate both foods immediately, perception of fullness immediately after the
meal was higher. Either way, supine is better than seated upright for
slowing gastric emptying and enhancing satiety.
Additionally, Murdoch, Fisher, and Hunt tested
subjects drinking a saline (salty water) drink sitting, lying on the left
side, or lying on the right side [115]. At 10 minutes after
ingestion of 750 ml., there was 215 ml. left from subjects
lying on the right side, 431 ml. left from subjects lying on the left side
(P < 0.005), and 308 ml. left from the subjects sitting erect.
So lying on the left side is much more effective than sitting erect, and
sitting erect is more effect than lying on the right side. However, in a
similar experiment with 750 ml. of water with glucose monohydrate, there
was no statistical difference between groups. Another study with a
low-nutrient soup ingested with olive oil showed emptying
occurs more slowly, and hunger was reduced when subjects were
lying on the left side than when they are seated [116]. These authors
propose that that gravity slows emptying when subjects are on the left
side or supine because of the anterior position of the antrum and pylorus
relative to the body of the stomach. They also suggested that nutrients
such as glucose, which strongly activate intestinal receptors, offset any
slowing of gastric emptying by gravity.
Posture has little effect on digestion when solid
foods are digested without liquids [117].
Fiber
Dietary fiber is poorly
digested; this results in an accumulation of material in the small
intestine and subsequent delay in nutrient absorption [119]. Howarth,
Saltzman, and Roberts demonstrated that an additional 14 grams of fiber
results in a 10% decrease in caloric intake [120].
Fiber also enhances CCK.
Having fat and fiber slows the disappearance of lipids from the small
intestine, increasing the release of CCK [122]. The addition of barley to
a low-fat meal has been shown to have similar effects [123], and having
beans as a source of fiber doubles the body’s response to cholecystokinin
[124].
Many other studies show fiber will enhance insulin
sensitivity, increase adsorption, delay small intestine transit time, slow
gastric emptying, promote viscosity, and much more [126]. The subject of
fiber has been covered in previous issues of JHR. For more on this
subject, read
Fiber Dynamics Part I
Fiber Dynamics Part II. Also, if you are just starting to
supplement with fiber, increase it slowly to avoid gastrointestinal
distress [121].
Energy (Calorie) Density
Here is a quote from the current writer to introduce this term [127]:
“Q. What is calorie density?
A. Calorie density (CD)
is the number of calories per weight of food. A perfect illustration is
found when comparing proteins, carbohydrates, and fats. Typically,
proteins and carbs contain 4 calories per gram, while fats have 9 calories
per gram. Fats would be said to have a higher calorie density than the
former two.”
Many scientists would claim that energy
density is the most potent weapon one has for manipulating satiety [121].
This topic has been highly investigated by nutritionists, and results
support the claims made. For example, Duncan, Bacon, and Weinsier, over 5
days, gave 20 obese and non-obese subjects a diet low in energy-dense
foods and one high in energy-dense foods and then allowed each group to
eat until satisfied [128]. The subjects which ate as many low-energy dense
foods as they wanted had 1,570 calories, while the subjects which ate
high-energy dense foods had 3000. Furthermore, the former group ate 33%
longer throughout the day than the latter group.
Water content also effects energy density
and can influence hunger. For example, Bell et al. gave subjects a
milk-based drink or no drink (control), followed 30 min later by a
self-selected lunch, and 4 hours later by a self-selected dinner [129].
The milk drinks were equal in energy and macronutrient content; the only
difference was they added water to increase the density to 300, 450, and
600 ml. The participants significantly reduced subsequent
intake after the 600 ml milk drink compared to the 300 and 450 ml drinks,
showing that adding water to food can be of great value to a dieting
individual.
Now, the question remains of whether having
water on the side with solid food effects hunger equally to mixing it with
a solid food or energy-dense liquid. To test this, Barbara and company
gave their subjects 1 of 3 isoenergetic (1128 kJ) preloads 17 min before
lunch on 3 days and no preload on 1 day [131]. The preloads consisted of
1) chicken rice casserole, 2) chicken rice casserole served with a glass
of water, and 3) chicken rice soup. The soup contained the same
ingredients (type and amount) as the casserole that was served with water.
Results showed that decreasing the energy density and increasing the
volume of the preload by adding water to it significantly increased
fullness, reduced hunger, and subsequent energy intake at lunch (26% less
kcals were consumed). The equivalent amount of water served as a beverage
with a food did not affect satiety. So according to this study, mixing
food with water, such as a protein shake, will affect satiety, but having
a glass of water and some steak, for example, will have very little
additional benefit to hunger than having the steak by itself. Adding water
on the side with food has conflicting results, however. For instance,
women served breakfast with or without two glasses of water showed that
consumption of the water decreased hunger and increased satiety during
breakfast, but this effect did not extend beyond the meal [132]. In
conclusion, mixing water with food is very well-established for decreasing
hunger. Having it on the side is not, but it certainly would not hurt to
have some, not to mention the anabolic effects of staying hydrated. The
authors postulated that the results could be that water in food increases
the weight or volume of the food and changes the dispersion of nutrients
consumed, probably activating mechanisms involved with hunger. On the
other hand, water consumed on the side would be processed by thirst
mechanisms, which are distinct from those for hunger [131].
Additionally, adding fiber to meals
(low-calorie, lowering energy-density) significantly decreased caloric
intake in lean women [130].
It has been suggested that density could
affect satiety through mechanoreceptors (relay mechanical stimuli
information in the nervous system, such as hair cells, which help hearing)
or chemoreceptors (detect chemicals and relay information in the nervous
system, such as taste) in the oropharyngeal (around the throat) or
gastrointestinal tracts. Additionally, the volume of food could influence
satiety by affecting the perception of how much has been consumed. People
may equate portion size with energy content and adjust subsequent intake
accordingly [133].
Because of these results, it has been
postulated that carbs and proteins have higher satiating effects than
fats, and the results do indeed support this. We will be discussing this
further on in the article.
Volume
As discussed previously, energy density (kJ/g) of
foods strongly affects satiety. However, the question still remains
whether increasing the volume or size of a food, independent of weight,
affects hunger. To test this, Rolls, Bell Bethany, and Waugh fed 28 lean
men breakfast, lunch, and dinner in a laboratory 1 d/wk for 4 weeks [118].
They gave them isoenergetic (equal amount of energy), yogurt-based milk
shakes that varied only in volume (300, 450, and 600 ml) as a result of
the incorporation of different amounts of air. The food contained
identical ingredients and weighed the same. The high volume drink
significantly affected energy consumption at lunch. Energy intake was
approximately 12% lower after the 600 ml drink than after the 300 ml
liquid. Subjects also reported greater reductions in hunger and increases
in fullness after consumption of both the 450 and 600 ml drinks than after
the 300 ml ones. Therefore, varying the volume (irrelevant to weight) does
affect satiety and digestion.
This experiment should have profound effects on the
nutrition industry. This means that foods such as popcorn, which are very
light but puffy because of air volume, have higher satiety than foods with
the same weight and energy but less volume. Designing foods with high air
volumes would therefore assist a great many of dieting customers;
likewise, when dieting, consuming high-volume foods would be of benefit to
the athlete.
Exercise
Training can have varying results on hunger.
Initially, exercise produces an anorexic effect. Moreover, the higher the
intensity, the more pronounced this effect is. In male rats, intense
exercise suppressed more food and caused more weight loss than
less-intense exercise [134]. In humans, results are very similar [135].
For example, King, Burley, and Blundell collected 23 healthy, lean, male
college student/staff members and randomly assigned them to a control,
low-intensity and high-intensity exercise treatment in the first study,
and to a control, short-duration and long-duration exercise treatment
(high intensity) in the second [136]. Hunger was significantly suppressed
during and after intense exercise sessions, and more so than low-intensity
workouts. This was a very short-term influence, however. Exercise had no
effect on the total amount of food consumed, but it did delay the start of
eating during the first meal. In studies in which a test meal was offered
50-75 min after exercise, appetite is not suppressed [137]. So
results are consistent that exercise promotes an initial anorexic effect,
but this is short-lived, and appetite resumes as normal thereafter.
Mechanisms for this short-term anorexic effect are
not completely understood; however, some authors postulate that hormones
such as cortisol, catecholamines, and the adrenocorticotrophic hormone
(ACTH, which stimulates the release of glucocorticoids) could cause this
[138, 139]. Perhaps the best known mechanism is CCK. Cholecystokinin
levels quickly rise during intense exercise, and since it its anorexic
effects are very short-lived, this would fit rather nicely with the above
observations [140]. Additionally, hypoxia (reduction of oxygen supply
to tissue below physiological levels) promotes a potent anorexic effect
[141].
Training’s long-term influence on hunger is a
different subject. One theory—the glycogenostatic hypothesis—states that
individuals consume food to a level that maintains glycogen levels in the
body. Results show, however, that glycogen stores themselves only have a
minor impact on hunger [142]. Conversely, glycogen depletion may
indirectly promote hunger, causing disruptions to occur in the
relationship to patterns of blood glucose and spontaneous meal initiation.
For example, Kathleen et al. had 10 men (age 20-31 yr) perform
glycogen-depleting exercise in the evening, eat a low-carbohydrate dinner,
and stay overnight in the laboratory. The next day, blood glucose was
monitored continuously. Subjects had access to high-fat and
high-carbohydrate foods after baseline glucose and respiratory quotient
were determined. Lastly, in the afternoon, 1 h of moderate-intensity
exercise was performed. What was interesting is that, in a state of
glycogen depletion, the subjects had blood glucose stability for two
meals. They consumed four high-carbohydrate sandwiches and 350 ml of a
high carbohydrate beverage. After this, the normal fall in blood glucose
before the onset of a meal and elevation afterwards returned to normal. In
total, 8 of 10 meals were initiated during instability in blood glucose,
which is very statistically significant. It is postulated that the reason
blood glucose did not decline before meal initiation in a
glycogen-depleted state was because the liver switched from retaining
glucose to releasing glucose, preserving blood levels. This decline in
liver glycogen, however, may be detected by peripheral and central nervous
system glucoreceptive elements, and mapped into meal initiation as stated
earlier. Initially low rates of glucose utilization could have been due to
high free fatty acid concentrations, and low insulin concentrations.
Lastly, a negative energy balance caused by exercise,
a decreased energy intake, or a combination of both, suppresses nocturnal
leptin secretion. While a positive energy balance, enhances leptin. This
would certainly effect satiety.
Cravings
Some unconditioned, innate senses of taste humans
have are preferences for sweets, avoidance of bitter foods, and a salt
appetite [144]. Furthermore, people tend to over eat sweet and
calorie-dense foods, while under eating unpalatable foods [147]. Other
foods are learned and selected according to experience. Four factors which
affect food intake are: olfactory (of, relating to or connected with the
sense of smell), orosensory (relating to or associated with eating or the
sense of taste, texture), sight, and postingestive stimuli (the effects of
foods after ingested). If something smells good, looks good, and tastes
good, you are more likely to eat it. From this, you can learn to crave
certain foods, and likewise learn to avoid certain foods which do not
taste, smell, or look good.
Moreover, hunger for certain macronutrients may be
mediated by neurotransmitters/modulators. For example, Barton, York, and
Bray injected galanin into the lateral cerebral ventricle of rats, and
salin into a control group. The galanin group consumed a very high fat
diet in response to this. Similar experiments show NPY promotes carb
consumption, and serotonin both proteins and carbs [145]. This theory
still needs more research, however, and results vary. Nevertheless, there
is a strong possibility that being deficient in any macro will promote
cravings in that particular macro. Moreover, being deficient in a macro,
such as carbs, will induce NPY synthesis, which will further promote
strong urges to eat. The craving for carbs in this case may be a learned
one, as eating them will decrease NPY mRNA, and subsequently relieve your
hunger pangs. Another example would be blood sugar; this is most likely a
learned desire from experience, to ingest carbs in response to low blood
sugar.
Postingestive stimuli are powerful factors. If you
eat a certain food and it gives you food poisoning for a night, you may
avoid that food for a long time, even though it may have been a freak
accident. Perhaps the most important postingestive factor for bodybuilders
though, is an analysis of their ABC (antecedent, behavioral,
consequences). For an explanation on this term, read the introduction to
Glutamine: the Conditionally Essential Amino Acid. The antecedent for
a bowl of ice cream is mixed: it tastes good, but it will also destroy my
gains. The behavior can vary because of this. If on a diet, an athlete may
break down and go on an ice cream binge; the consequence would be gaining
fat, and depression because he/she cheated, etc. For the most part, a
hardcore athlete will stick with the latter antecedent, and realize that
ice cream is an enemy to his/her body. In fact, many athletes claim to
hate greasy, cheat foods after avoiding them for years, so this makes it
easy for them. With this in mind, the athlete will avoid eating junk food,
and reap the gains of a strict diet.
Another example may be oatmeal. To most normal
people, this food tastes disgusting, but it is a staple in any
bodybuilder’s diet. Many athletes now actually enjoy the taste of a nice
bowl of oatmeal, and even prepare special dishes with it, such as oatmeal
mixed with cottage cheese. The athlete knows that this food is great, and
may learn to like it (antecedent); furthermore, they will behave by
ingesting it frequently, and the results will be very rewarding.
Focus
Cognitive (thinking) distractions have the ability to
increase meal intake; likewise, eliminating distractions can cause the
meal to be more satiating. Bellisle and Dalix demonstrated this on a group
of healthy women [149]. They separated them into several conditions:
condition 1, subjects ate alone (baseline); condition 2, subjects ate
alone while listening to recorded instructions focusing on the sensory
characteristics of the foods (attention); condition 3, subjects ate alone
while listening to a recorded detective story (distraction); and condition
4, a group of 4 subjects had lunch together. The same food was presented
to all parties. Meal size was significantly higher in the distraction
condition than at baseline (mean difference from baseline: 301 ± 26 kJ).
The group eating together and attention group had only a few increases in
meal size. Listening to something distracting or watching something that
catches your attention—such as pumping iron—can therefore help you finish
meals on a bulk by waving your attention away from the food. On the other
hand, when cutting, you should turn off the T.V and focus on your meal,
really enjoying every bite of it.
Artificial Sweeteners
Rogers and Blundell showed that a food mixed with
saccharin (an artificial sweetener) had little satiating capacity in
comparison to a meal sweetened with glucose or sucrose [150]. Canty and
Chan further compared the effects of aspartame, saccharin, and sucrose on
hunger and food intake [151]. They had a group of 20 normal adults consume
a standard breakfast, followed 3 h later by 200 ml of either
water or a sweetened drink. After this, the subjects recorded every half
hour hunger ratings. Hunger wise, the highest rating was given for water;
the non-calorie sweetened drink was a bit lower, but not statistically
significant; while the sugar was much lower, and had a high statistical
significance.
Overall, most the studies have shown that artificial
sweeteners either very slightly decrease hunger or do not affect it at all
[153]. So supplementing with them will have little benefit when dieting.
The only advantage would be to relieve a quick sweet tooth, but nothing
more. When bulking, however, adding artificial sweeteners to a plain food
such as oatmeal can enhance its palatability, and increase appetite [154].
In addition to this, artificial sweeteners have not been shown to increase
weight or fat gain in humans.
For instance, in order to test whether artificial
sweeteners increased fat gain in a long term study, Raben et al. fed
overweight men and women for 10 weeks with either sucrose or artificial
sweeteners everyday [152]. The sucrose group had increased energy intake,
body weight, and fat mass, while these effects were not observed in a
similar group of subjects who consumed artificial sweeteners.
Therefore artificial sweeteners do appear safe as far as weight gain is
concerned.
Sensory-Specific Satiety
The sensory-specific satiety theory states that one
is more likely to consume a higher amount of food if their diet has
variety, than one who consumes the same foods day in and day out because
of an adaptation in the senses to foods[160]. There are hundreds of
experiments which support this theory.
When animals are given a diet with a variety of foods
to consume, and a diet in which they can either consume one food or the
same type of diet consistently, the former group consistently is
hyperphagic compared to the later group [161, 162, 163]. Furthermore,
animals given several types of high-fat foods eat more grams and calories
than animals given one type of high-fat food [164, 165]. Having the same
food, but varying its composition also has the same effect. For example,
several experiments demonstrated that serving a group one food, compared
to serving a group the same food but with vanilla, lemon, and a variety of
other flavors, lead to the latter group having more calories and consuming
more grams than the other group [166, 167, 168].
Additionally, having more variety within one meal
promotes hyperphagia. For instance, Rolls et al. fed participants four
courses, one each of sausages, bread and butter, chocolate dessert, and
bananas, or four courses of one of these foods [169]. Those who had
variety each meal consumed 44% more food and 60% more energy than the
other group. Moreover, people given three flavors of yogurt over several
meals, compared to people with one choice, consumed a significantly
greater amount of calories [170]. In another experiment by Roll et al., he
gave his participants cream cheese sandwiches, and the only difference was
that he gave one group several of the same sandwiches with different
toppings: salt, lemon essence and saccharin, or curry [172]. The variety
group consumed 15% more calories than the plain one. There are hundreds of
other testimonies to substantiate this; however, there is a limit. If the
difference is too minor, over eating will not occur. For example, giving
people strawberry, raspberry, and cherry, with the same color and texture,
did not result in increased caloric intake [171].
The authors attribute this to an adaptation in the
senses. Having the same food over and over again decreases the
palatability and excitement during ingestion. Smelling, and tasting the
same food basically becomes a bore; however, when mixing it up, your
senses stay sharp and foods are easily consumed.
This has profound effects on bulking and cutting
cycles. When cutting it would be best to stick with the same foods, the
same texture, and makeup, etc. Only have a couple of carb sources, a
couple of protein sources, etc. But when bulking, the more variety the
better. When you have oatmeal, make oatmeal cakes, oatmeal shakes, oatmeal
cooked, oatmeal pancakes, etc. You want a variety of foods as well; have
yams, wheat bread, beans, steak, chicken, etc. Mix it up as well; have
burgers, chicken and oatmeal, beans and steak, etc. Now, you can still
have some variety during a cut, and you can stay basic on a bulk; this is
just another weapon placed at your disposal—use it wisely.
Fats, Carbs, & Proteins
Now its time to tie it all together and show which
macronutrient is the most satiating of them all. There is no straight
forward answer to this. All three are vital to one’s diet, and deficiency
in any, as displayed above under cravings, can and will promote hunger.
With this in mind, the results show proteins are most satiating, although
carbs often come a close second, and some studies (such as the satiety
index, discussed further on) show carbs to be number one. Fats are last in
just about every case.
First, a major reason fats have less satiety is
because they are so energy dense (discussed above). One gram of fat has
nine calories, while protein and carbohydrates only have four calories per
gram. Therefore, fats are often overeaten. Because of this, the majority
of journals recommend a low-fat, high-carb/protein diet for obese
individuals [174]. In one experiment, obese people were allowed to gorge
themselves on either high-fat or high-carbohydrate foods [175]. Obese
subjects voluntarily consumed twice as much energy from the
fat, displaying the weak satiating action of lipids.
Johnstone, Stubbs, and Harbron compared all three
macros in a study [177]. They gave subjects a high-protein (HP), fat (HF),
or carb (HC) diet, and compared hunger and satiety throughout the day.
Participants on the high-protein diet felt less hungry and fuller than the
other two diets, and the high-carb diet had better results than the
high-fat diet. Moreover, the HC diet was more satiating than the HF diet
after each meal.
Plantenga et al. composed an experiment to assess a possible relationship
between perception of satiety and diet-induced thermogenesis (DIT; this is
a whole other subject, which will be talked about in the future, but fats
give very little DIT, while proteins and carbs do) [178]. The subjects
were eight females, ages 23-33. Subjects were fed a PCF of 29/61/10 and
9/30/61 with all other conditions being equal. Thermogenesis was higher on
the high protein/carbohydrate diet, satiety was higher during meals (P <
0.001; P < 0.05), as well as over 24 h (P < 0.001), than with the high fat
diet. These results showed a high carb/protein diet will elicit s much
higher satiety and DIT than a high fat diet.
In another study, after a lunch, Marmonier, Chapelot,
and Sylvestre gave subjects a high-fat (58% of energy from fat),
high-protein (77%) or high-carbohydrate (84%) snack, and than viewed how
long they waited until dinner [179]. Consumption of a high-protein snack
delayed the request for dinner by 60 min. In contrast, a high-fat snack
delayed dinner request by 25 min, whereas a high-carbohydrate snack
delayed dinner request by 34 min. Snack composition had no impact on
energy or macronutrient intakes during dinner. Another experiment on
snacking showed similar results, except the delay in meal request was
less. Furthermore, the calories consumed at dinner were not suppressed
[180]. The authors concluded that snacking has poor satiating efficiency,
and may play a role in gaining excess weight. So one should be careful
with excessive snaking, and instead opt for full, balanced meals.
There are many other studies like this. In
conclusion, proteins appear to have the highest satiety point, then carbs,
then fats. You can certainly see yet another logical reason to follow a
high-protein diet, as most athletes do.
Fat Chain Length
In order for a bodybuilder to get a proper amount of
fat in their diet, they must add specific fatty foods such as peanut
butter, flax, safflower, etc. There are a variety of fats, including
saturated fats, polyunsaturated fats, and monounsaturated fats. These fats
vary in level of satiety though.
In order to see which fat was most satiating, Lawton
et al. composed an experiment on two different groups of 20 subjects each
(half male and female) [173]. Group one tested the effects of fat A (oleic
blend, high in monounsaturated fatty acids (MUFA)) with those of fat B (linoleic
blend, high in polyunsaturated fatty acids (PUFA)) and fat C (stearic-oleic
blend, high in saturated fatty acids (SFA)). Energy and nutrient intakes
were monitored for the rest of the day and for the following day. Profiles
of hunger, fullness, and other sensations were monitored by continuous
tracking and end-of-the-day questionnaires were filled out. Subjects
consumed significantly more energy after consumption of the lunch
containing fat A (MUFA), and were hungrier than after the lunches
containing fats B (PUFA) or C (SFA), and there was a trend for these
effects to continue into the second day. Lastly, fats B had a higher
satiety than fats C.
A second study was designed to confirm and extend the
findings of Study 1. It compared the effects of fats A, B, C, and
additionally, fat D (a linoleic-oleic blend). In Study 2, fat C produced
similar effects on appetite to fat A, and there was a tendency for
subjects to consume more over the whole test day when they had consumed
the lunch containing fat A than when they had consumed the lunch
containing any other fat. Additionally, they prolonged this study for 40
days, and the results of test one were confirmed.
Therefore, when bulking you would want to consume a
lot of monounsaturated fats such as peanut butter, and when cutting you
would want to lower your intake of peanut butter (among other monos) and
opt for polyunsaturated fats, such as flax and safflower
Now, while you can vary your fats a bit, you still
need to maintain a proper essential fatty acid ratio. Read the following
article for instructions on that,
Essential Fatty Acids - An In Depth Analysis
High- vs. Low-GI Carbs
Carbs are often measured by the glycemic index (GI).
The higher the GI, the simpler and fast-burning the carbohydrate is; the
lower, the slower burning it is. In terms of maintaining a steady flow of
blood glucose, you definitely want to opt for low-GI carbs throughout the
day (save post-workout); however, in the short-term, high-GI carbs are
more satiating than low-GI carbs.
For example, Anderson et al. gave subjects high-glycemic-index
preloads (glucose, polycose, and sucrose) and low-glycemic-index preloads
(amylose, amylopectin), then measured hunger ratings and how much they ate
thereafter [176]. Carbohydrates with a high GI were more satiating, and
suppressed hunger much more than low-GI carbs. Other studies also testify
to glucose’s anorexic effects within 1 hour of consumption [91, 92].
Some reasons for these effects are that insulin is
very satiating, NPY would be reduced, blood sugar would be initially
higher, nutrients would be delivered quicker, etc. So in the short-term,
having a post-workout shake, for example, would be more satiating than
oatmeal. High bursts of insulin (induced by high blood sugar) promote
hypoglycemia, however. Soon you would get very hungry because of low blood
sugar; therefore, you want to have slow-burning carbs throughout the day.
On a bulk, however, high-GI carbs may be of benefit. This is discussed
further on under practical applications.
Starvation
Some people are hungry because they basically starve
themselves. This is why it is important to understand how LBM, height,
weight, etc. affect your metabolic rate. For one athlete, 2000 calories
may be more than adequate for hunger, health, etc. For another athlete who
has twice as much muscle mass, for example, that would be pure starvation
and result in constant hunger. Further, as stated above, leptin, CCK,
etc., are much less effective and concentrated in the body on a starvation
diet. Furthermore, NPY, among other orexigenic factors, will be
skyrocketed. I recommend you read
13 Weeks To Hardcore Fat Burning - "The Diet" to understand
how to calculate how many calories you need, and follow the many safe tips
for dieting given within.
Other Factors
There are many other factors than an actual
physiological need for food that must be considered. People may not
consume food because of cultural background, social situations, pressures
to look thin, or to fit in with the crowd, which leads to ailments such as
anorexia. You could simply have a bad habit, or you could lack any
self-discipline and be a lazy, fat, slob.
People tend to eat more in cold weather and less in
hot weather [155]. This has given credence to the thermostatic hypothesis,
which states that the hypothalamus regulates body temperature and food
intake, and proper interaction of temperature and eating behavior [156].
External factors such as smell can influence
appetite. Appetite is the physiological desire to eat in relation to
sensations for foods, while hunger is a physiological need to eat. So
while you may have appetite, your body might not actually need that food.
A good example would be if you have a huge bowl of oatmeal, steak, a
salad, and some essential fatty acids. At the end of this meal, you would
feel stuffed and no longer desire to eat anymore oatmeal or steak.
However, you may have an urge to down a nice, palatable bowl of ice cream.
That is appetite—not hunger.
Environment is vital to one’s success. If you wake up
every morning to a box of Krispy Kremes or the smell of freshly baked
cookies, you are much more likely to cheat. If, however, you only allow
clean foods in your household, such as oatmeal, cottage cheese, peanut
butter, whey protein, etc., appetite will be greatly suppressed and, even
if you do cheat, a couple bowls of oatmeal will not hurt your diet—in
fact, it may help. A Krispy Kreme, on the other hand, is absolutely
worthless and will only hurt your body. So I would encourage you to
surround yourself with less-tempting foods. Whomever you live with, or
work with, try to get them involved in healthy eating. Having people
around that support your goals is vital to any bodybuilder’s success.
Several studies have shown that stress can promote
anorexia [157]. It is postulated that corticotropin-releasing
hormone (CRH) and/or serotonin (5-hydroxytryptamine, 5-HT)
contribute to this [158]. Both are anorexigenics, and elevate in response
to stress throughout the brain, including feeding centers. Additionally,
CRH inhibits NPY release [159].
In other situations, such as depression, emotional
breakdowns, lowliness, etc., people may react by overeating.
Should You Ignore the Hunger Mechanism?
No, you should not ignore it. If you feel excessively
hungry, or anorexic, you need to take a close look at your diet and
analyze your weak points. You may have low blood sugar, or NPY may be high
due to low-carb dieting. You may be low in fat or protein. You may not be
having enough fiber or low energy-dense foods, etc. There are many tricks
to manipulating hunger. After reading this article, there is little excuse
left not to get the job done and eat the amount of calories necessary to
get you optimal results, without feeling excessively uncomfortable when
cutting or bulking.
Other Bodily Factors Which Regulate Hunger
There are literally hundreds of other hormones,
peptides, and endo/neurological signals to be discussed, but this can be
written about for years on end and through hundreds of papers. In fact,
millions of scientific journals are composed on this very subject, and
scientists still do not fully comprehend the marvels behind hunger
regulation. So to close this out, I am going to give you a quick wrap up
on a few more peptides an |
