Part 3-Appetite
In part 1 and parts 2a and 2b of this series we went over what some of
the research shows and how this runs counter to what most people are told and
end up doing to lose weight. Here’s a
recap:
A calorie is indeed a calorie, but your body doesn’t use
calories. A Calorie is a measure of
things your body uses, namely carbohydrates, protein and fats. However, what you eat is not merely energy,
it is raw materials for cell membranes, hormones, enzymes and a host of other
important chemicals and structures
As you lose weight by lowering calorie intake, your body
lowers your metabolism making the calorie you burned when you started much
easier to burn than the calorie you burn after dropping 50lbs. Conventional wisdom is that this is a result
of your body protecting body fat stores for times of famine. However, if you overconsume calories, your
body will actually increase metabolism and in both instances it is capable of altering
metabolism by 25%. If your body truly
was trying to conserve energy, why would the rules change when you are eating
to excess?
Obviously your body adjusts metabolism to the energy intake
you provide it with. This is your body
adapting to the environment it is in. If
you provide too much energy, your body increases energy output and when you
decrease energy your body lowers energy output.
Looking at it in terms people can understand, which car do you have more
faith in, one that can go 500 miles on a tank of gas or 400 miles? Assuming they are identical, you have to
wonder where all of the extra energy is going in the less efficient car since
it is not being used for driving further.
In humans, it’s quite possible that the extra energy is speeding up all
of your body processes, which is not good.
Efficiency is good, especially when you are dealing with your body, cell
division, and repair processes.
While some of your cells will only run on glucose, it is not
the preferred fuel for your body. Your
body’s preferred fuel is based on what you put it through via the day, i.e.,
your environment. If your job or life is
filled with a lot of high force activity, glucose is your body’s preferred
fuel. If you are part of the 99% of
people in the United States that sit for hours at a time, drive an hour to
work, and only bend over to pick up the piece of donut they dropped, this
doesn’t apply to you and fat is your guy.
Mismatching fuel to both what you are engineered to run on
(Your genes) and the type of activity you perform drives obesity and diabetes.
Diet is not the only player in this story, exercise is a
significant player as well. When your
diet doesn’t match your activity type and level, insulin is used to shuttle
glucose in to your muscle and liver cells for storage. It isn’t that insulin is a bad thing, if you
look at Type 1 Diabetics who don’t produce any, you can clearly see how
important it is. The problem with
insulin is when we rely on it as the primary way of getting glucose out of our bloodstream
and in to our cells. Once your cells’ glycogen
stores are full they stop listening to insulin and you begin to convert the
glucose to fat. High levels of insulin
help shuttle this fat in to your fat cells.
Exercise also shuttles glucose in to the cells but instantly burns
it. Provided the intensity of exercise
is sufficient, exercise also empties glycogen out of muscle cells and improves
their sensitivity to insulin, making it less likely glucose will be turned in
to fat and stored. In the long term,
exercise also increases the amount of glucose your body can store as glycogen,
allowing a higher consumption of carbohydrate before conversion to fat.
Control of appetite
Now that we have gone over the way our muscles use fuel, we
need to direct our attention to appetite.
The primary difference between us and a machine with regard to energy is
that we are capable of providing ourselves with energy, and the signal to do
this is via appetite. Appetite is dictated
by the interplay between the hypothalamus in the brain, the gastrointestinal
tract, and adipose (Fat) tissue. Both
hormones as well as circulating levels of glucose and fatty acids provide
information to the hypothalamus so that appetite can be adjusted. The primary hormones that deal with
regulating appetite are Ghrelin, PYY, Leptin, and insulin.
Ghrelin is a hormone secreted by the empty stomach to
stimulate food uptake. Once you eat and
the food enters your stomach, ghrelin release is stopped, signaling you to stop
eating. PYY, on the other hand, is
released after you eat to signal that you are in a fed state and can stop
eating. Both of these hormones work by
controlling the secretion of appetite stimulating Neuropeptide Y and AgRP; ghrelin
by increasing secretion and PYY by inhibiting it. Leptin, on the other hand, is a completely
different animal.
When you consume too much food, whether it is from fat or
carbohydrate, the excess energy is converted in to fat. As you starting making triglycerides, the
storage form of fat, they move to adipose tissue where they are stored. This releases the hormone leptin from the
adipose tissue, which signals the hypothalamus to decrease appetite. In the short term, insulin tends to signal
the hypothalamus to curb appetite in a similar way. In the long term, high levels of insulin seem
to have the opposite effect, increasing appetite.
Leptin resistance
As your body fat increases, it secretes more leptin to
signal a fed state. While body fat
increases you become insulin resistant, and as this body fat continues to
secrete leptin, you actually become leptin resistant. In a healthy individual, the hypothalamus
gets the signal that high levels of leptin mean you no longer need to eat, but
in the leptin resistant individual, the cells within the hypothalamus either
don’t get the signal or ignore it. Despite
having high levels of circulating leptin, obese individuals that are leptin
resistant do not get the fed signal and their appetite remains high. It’s not that they are always hungry, it’s
that they never get the signal to stop eating.
As you can see, leptin resistance and insulin resistance run hand in
hand with one another. If you can
control insulin resistance you can control leptin resistance, allowing your
hypothalamus to properly control appetite.
This is by no means a comprehensive list of hormones within
the body that control appetite, but these are the major players. As mentioned above, circulating levels of glucose
and fatty acids also play a major role in the regulation of appetite. In fact, if you are insulin resistant, the
nutrient partitioning (Fuel selection) effects of insulin can boggle this
signal and not only inhibit fat loss, it can also make the effects of cutting
your caloric intake unbearable.
Trappings of caloric restriction
Anyone who has undertaken a weight loss program by either
reducing calories or exercising away the pounds has at one time felt
voraciously hungry, irritable, dizzy, brain fog, or just a complete lack of
energy. Eventually you reach a tipping
point and go on a food binge, undoing most of the weight loss progress you have
accomplished up until that point. Most
of this can be very easily explained when you look at what you eat, not
how much.
When most people decide to tackle a weight loss program,
they will cut their calories to some number, let’s say 1500, and begin
exercising. For the most part, people
will keep their carbohydrates at 50% of their calories which leaves them with
187.5 grams of carbohydrate. It has been
established that when the brain and central nervous system use glucose as their
primary fuel, they need approximately 150g for proper functioning. This leaves 37.5g of glucose for the rest of
your body to use. The problem with this
situation is that even just taking resting metabolism in to account, this is
not enough. So, not only are you already
starting out in a hole, once you exercise you have depleted some of the glucose
that would be later used for the brain.
A 130lbs woman will burn approximately 60g of glucose during
an hour long run at a pace equivalent to a 10 minute mile. Increasing the intensity you run at not only
increases the amount of carbohydrates you burn via an increased calorie burn,
it also increases the percentage of carbohydrate you burn, a double
whammy. This energy is taken out of the
system as it is performed, so the brain will eventually enter a low energy
state unless you provide it with more fuel.
Just taking in to consideration total daily carbohydrate intake and not
accounting for the fact that this exercise may have been done while you have
only consumed 1 or 2 meals, this leaves you with 127.5g of carbohydrate for a
system that needs 150g. Interestingly
enough, this system also contains the appetite center.
Your brain on ketones
As you can see, a single exercise session of an hour can
cause your brain to enter a low energy state while carbohydrate is the dominant
fuel source, leaving you hungry and negatively impacting brain function. This doesn’t even take in to account the
glucose that is used for other parts of the body that can only run on glucose
as well as other physical activity you may take part in. It is very easy to see how this could leave
you feeling hungry, irritable, preoccupied with food, and a little off
mentally. All is not lost, however. While it was thought for many years that the
brain could only run on glucose, there is actually another fuel the brain can
use. The best part about this fuel is
that you will not run out of it until you run out of body fat. This fuel is a byproduct of fatty acid
metabolism called ketones.
Most people familiar with the Atkins diet have heard of
ketones or ketosis. Ketones are
essentially the leftovers once a fatty acid has been metabolized for energy and
can be metabolized for energy by the heart and the brain. With ketones provided as an energy source,
the brain can function on less carbohydrate, allowing the rest of the body to
use what it needs without negatively impacting brain function. As a substitute for glucose, ketones can
provide up to 70% of the brain’s energy needs, lowering the amount of glucose
necessary for proper function from 150g to 45g.
Provided you have a good amount of fat to lose, the brain will not enter
a low energy state until those fat stores are gone, which is more or less the
point of a fat loss program.
The question now becomes, “How do we get the brain to run on
ketones?” In a healthy individual who
has good insulin sensitivity and who exercises regularly, ketones probably
provide some energy for the brain. In an
insulin resistant individual, high levels of insulin prevent ketones from being
formed by blocking the release of body fat stores AND inhibiting fat
burning. In addition, having a high
level of carbohydrate in the diet while at the same time eating every 3 hours
will cause insulin to be secreted for a couple of hours after every time you
eat, which brings us to another myth.
Eating every 5 hours is foolish and will not dramatically impact your
metabolism. In fact on a moderate to
high carbohydrate diet it will do more harm than good.
The thermic effect of food, the number of calories used to
process what you eat, is related to the amount of food you eat, not how many
times you eat. For comparison’s sake,
the thermic effect of food only accounts for 10% of the calories you
consume. In someone who eats 2000
calories, that effect is 200 calories per day, so we are probably only dealing
with a 50 calorie per day difference between eating 5 times a day instead of 3
times. However, if you eat 5 times a day
and get insulin secretion for 2-3 hours after every time you eat, this will
lead to 10-15 hours per day that you cannot access body fat stores or burn fat effectively
to make ketones for the brain. This will
certainly affect appetite, talk about putting your eggs in the wrong basket.
Becoming keto-adapted
So, how do we get the body to become keto-adapted? First, you have to repair insulin sensitivity
to lower the amount of insulin coursing through your veins so that ketones can
be made. The most effective way to do
this is to reduce the amount of carbohydrate you consume for a few days. The amount of carbohydrate you should consume
is variable from person to person, but a general recommendation is under 50g of
carbohydrate for 2 weeks followed by a gradual increase to tolerable levels
based on activity level (1). Once you’ve
done this and things start working properly, keeping insulin levels low via
carbohydrate restriction and properly programmed exercise will allow ketone
bodies to be formed. In the initial
period following this adaptation, your brain is not very efficient at using
ketones. People who have done the Atkins
diet are probably familiar with ketosis and measuring ketones in your
urine. If you are dumping a significant
amount of ketones out of your body via urine, your brain can’t possibly be
using them effectively. In fact, once
your brain does start using them, urinary ketone levels should start to drop.
There is another way to get ketones to the brain without
consuming a low carbohydrate diet.
Coconut oil contains medium chain triglycerides(MCTs) which are
instantly metabolized for energy. As a
result, ketones are formed and can be used by the brain as energy, which may be
the mechanism by which coconut oil suppresses appetite. However, this effect will probably only work
on someone who is fit and has a properly operating metabolism. In other words, if you are insulin resistant,
it probably won’t work. If you are an
athlete with good insulin sensitivity, MCTs may be something you want to look
in to.
The benefit of ketones to the brain may be far greater than
the effect on appetite and body composition.
It has been hypothesized that the protective effect calorie restriction
has on the brain may be related to the use of ketones as a substrate. Increases in brain-derived neuroptrophic
factor (BDNF) that occur during fasting may be triggered by the ketogenic
energy pathway as are multiple other protective factors (2). BDNF is a potent driver of brain
neurogenesis, the ability to form new connections in the brain. From an evolutionary perspective this would
make sense, it is obviously beneficial for brain function to be enhanced when
food is scarce, and for the greater part of our evolution fasting wasn’t a
choice it was more or less forced upon us.
This is all speculation at this point, there have been no good trials
looking directly at ketones and neurogenesis in humans. The fact that the neuroprotective effects of
calorie restriction seem to be mirrored during a ketogenic diet provide some
support that it is not merely the reduction in calories that are the primary
driver.
Conclusion
Hopefully this 3 part series has given you an idea as to how
complex the science of weight loss and nutritional intervention is. While I agree that calories do matter,
looking at calories in vs calories out is far too simple of an algorithm to use
for weight loss, which is probably why it rarely works when you take in to
account all of the factors, including appetite.
We not only have to take in to consideration energy, we have to look at
the type of energy, the type of activity being performed, the machinery doing
the activity (Fiber type and cell type), as well as appetite. Taking a comprehensive approach is far more
effective than the generalist approach of using the energy balance equation,
especially when we are dealing with tissues and organs that can alter which
substrate they use for fuel depending on the fuel you provide. Improving insulin sensitivity via the
appropriate exercise and diet as well as getting the brain to run on ketones
puts more tools in your tool box.
Whether or not you are improving insulin sensitivity directly via
carbohydrate restriction or via calorie restriction is irrelevant, they both
will work and through basically the same mechanisms. However, given appetite is a major
consideration that will be negatively impacted by calorie restriction and
positively impacted by carbohydrate restriction, the scales easily tip in favor
of carbohydrate restriction.
References
