Engineer eats ONE KILO a month of Marmite | Daily Mail Online

Engineer eats ONE KILO a month of Marmite | Daily Mail Online

Is this Britain's fussiest eater? Engineer who
'hates food' and only eats 10 things says he is being kept healthy by
his ONE KILO a month Marmite addiction

• John Pearson from Burton-upon-Trent, Derbys, eats 1kg of spread a month
• Claims the yeast extract is the only reason he stays healthy 
• Will only consume plain crisps, cheese, chips and chocolate cake

By

Anucyia Victor for MailOnline

Published:
23:45 EST, 20 February 2015

|
Updated:
08:19 EST, 21 February 2015

423

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Meet the man who claims to hate food and says he is only kept alive by his Marmite addiction. 

John
Pearson claims he will only eat 10 bland foods - including plain
crisps, chips and chocolate cake - and has to top up his vitamin intake
by eating a kilo of the yeast extract.

The engineer, from Burton-upon-Trent, Derbys, says the love it or hate it condiment is the only reason he stays healthy.

+4

John Pearson says he hates food and is only being kept alive by his Marmite addiction

The 48-year-old spends a paltry £10 a week on his limited diet and was even nicknamed 'Breadroll' when he was at school.

Mr
Pearson said: 'Marmite has been my life-saver. I hate food. I don't eat
for pleasure, only because I'm hungry. I eat to stay alive.'

Mr Pearson's kitchen cupboards are virtually empty and he only keeps butter, cheese and milk in his fridge.

There is only bread in his freezer and his cupboards are home to his beloved Marmite and a couple of boxes of cereal.

'I go to the supermarket and buy everything I need for the week and it costs me about £10,' he said.

'Obviously, I get a massive jar of Marmite, loaves of bread, cheese and butter. I get some coke and skimmed milk.'

+4

The 48-year-old's fussy eating habits started when he was 18-months-old and has cost him two marriages 

Mr Pearson believes his problems with food started when he was just 18-months-old and a virus meant he vomited everywhere.

'I
got ill as a toddler and I think that's what triggered
everything.Before I got sick, I ate vegetables and fruit. I literally
had the same meals as my mum and dad but smaller.

'After
I got better, there was nothing I wanted to eat. All the food reminded
me of being sick. Mum tried everything to help me enjoy food but she
says I just wouldn't.

'I had an issue with colours and textures and I just couldn't eat it.'

As a child he dreaded lunchtime when the dinner ladies would force him to eat his school meal.

THE TEN FOODS JOHN WILL  EAT:  

• Milk
• Bread
• Cereal
• Coke
• Skimmed milk
• Plain crisps
• Chips
• Chocolate cake
• Butter
• Cheese

As he grew up Mr Pearson was warned that his poor diet could lead to blindness, rickets and scurvy.

John
said: 'I ate bread and butter and that was about all I could manage.
I'd sit there feeling really miserable just staring at my plate of food.
I knew I wouldn't be able to eat any of it. When the dinner lady took
my plate away I'd smile with relief.

'The head teacher at school called my mum in to talk to her about my eating habits.

'She was worried about how little I ate and my mum tried to explain why I hated food so much.

'She
told them about my illness when I was little. I don't think they really
understood but life got a whole lot easier when I got to secondary
school.'

+4

Mr Pearson gets ready to bite into a slice of bread and butter smeared with Marmite 

Hot meals - apart from chips - are out of the question. 

Mr Pearson does not eat vegetables or meat and hates a traditional Sunday lunch.

John
said: 'I have chips on a Saturday with my brother. But in the week, I
pretty much live on sandwiches or toast. I like bread and butter so
that's one good thing.

'When I get in from work, I have toast or Marmite sandwiches with a bag of plain crisps.

'Later in the evening, I might have some more.

'In the day, I sometimes have Marmite too. I eat at least one kilogram of the stuff every month.'

He is so fussy that his two ex-wives partly blamed his eating habits on their break-up.

 'I hate the fact that I hate food. It really does ruin things,' he said. 

'My issue with food was never the main reason why my marriages ended but both women said it was a contributing factor.

'I suppose living with someone like me, who has a huge problem with food, takes its toll.'

Mr Pearson rarely goes to restaurants and the most he can achieve is a pint in the pub followed by a bowl of salty chips.

Next month, his parents have invited him out to celebrate their 50th wedding anniversary.

John
said: 'Thankfully, my parents like one particular restaurant and
they've already asked if I can just have a plate of roast potatoes.

+4

The engineers said he will only
consume plain crisps, chips, chocolate cake, butter, cheese, milk,
bread, cereal, coke and skimmed milk

'I've been there before and I'm sure the staff will help me. They know that I'm fussy.'

Despite his huge food fetish, John has not passed his problem to his two children, Chloe, 21, and Michael, 20.

Mr Pearson  said: 'I remember once, when Chloe was just a baby, I was feeding her beans in her highchair.

'I
absolutely hate them but I was doing ok spooning them into her mouth.
Then the phone rang and distracted me. I picked up the phone and left
the bowl and spoon on the tray of her highchair.

'When
I got back, she flicked the spoon and it landed in my face. I had beans
all over my cheek and I literally froze. I ran upstairs, stripped off
all my clothes and got in the shower.

'Twenty
minutes later, when I was clean, I went back down to sort Chloe out.
She was crying by now and I felt awful, but I had to go and have a
wash.'

Sessions
of hypnosis and psychotherapy have failed to cure him but, despite his
food fad, he is fighting fit and is a 2nd Dan black belt in karate.

After sessions with a psychotherapist, he managed to eat raw carrots, grapes and bananas but couldn't keep it up.

 'I couldn't keep it up. I used to dread going home from work because I knew I had to try and eat some banana or grape,' he said

'Now I don't care. I am what I am and I can't change. I know I have a problem with food but I am too old to be cured.

'I'll stick to my 10 things and that will do for me.'

Read more: http://www.dailymail.co.uk/femail/food/article-2961506/Engineer-eats-ONE-KILO-month-Marmite.html#ixzz3SM8jbY8n

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▶ Astroturf and manipulation of media messages | Sharyl Attkisson | TEDxUniversityofNevada - YouTube

Published on 6 Feb 2015

In
this eye-opening talk, veteran investigative journalist Sharyl
Attkisson shows how astroturf, or fake grassroots movements funded by
political, corporate, or other special interests very effectively
manipulate and distort media messages.



Sharyl Attkisson is an
investigative journalist based in Washington D.C. She is currently
writing a book entitled Stonewalled (Harper Collins), which addresses
the unseen influences of corporations and special interests on the
information and images the public receives every day in the news and
elsewhere. For twenty years (through March 2014), Attkisson was a
correspondent for CBS News. In 2013, she received an Emmy Award for
Outstanding Investigative Journalism for her reporting on “The Business
of Congress,” which included an undercover investigation into
fundraising by Republican freshmen. She also received Emmy nominations
in 2013 for Benghazi: Dying for Security and Green Energy Going Red.
Additionally, Attkisson received a 2013 Daytime Emmy Award as part of
the CBS Sunday Morning team’s entry for Outstanding Morning Program for
her report: “Washington Lobbying: K-Street Behind Closed Doors.” In
September 2012, Attkisson also received an Emmy for Oustanding
Investigative Journalism for the “Gunwalker: Fast and Furious” story.
She received the RTNDA Edward R. Murrow Award for Excellence in
Investigative Reporting for the same story. Attkisson received an
Investigative Emmy Award in 2009 for her exclusive investigations into
TARP and the bank bailout. She received an Investigative Emmy Award in
2002 for her series of exclusive reports about mismanagement at the Red
Cross.



This talk was given at a TEDx event using the TED
conference format but independently organized by a local community.
Learn more at http://ted.com/tedx

▶ Astroturf and manipulation of media messages | Sharyl Attkisson | TEDxUniversityofNevada - YouTube

The Katering Show – WE QUIT SUGAR

Published on 10 Feb 2015

In
an attempt to live forever, and become just like their Instagram idol,
Sarah Wilson, McCartney and McLennan give up the sweet stuff; sugar.
Please Note: This episode is booze, sugar, gluten, fructose, lactose and
personality-free.



Get more Katering:

Explore Katering: thekateringshow.com

Follow Katering: twitter.com/thekateringshow

See Katering: instagram.com/thekateringshow

Like Katering: facebook.com/thekateringshow

Insulin: An Undeserved Bad Reputation, Part 5: Addressing the Critics » Weightology Weekly

Insulin: An Undeserved Bad Reputation, Part 5: Addressing the Critics » Weightology Weekly

This series on insulin
has stimulated numerous threads of discussion on various sites on the
internet.  I have seen some of these discussions and some unfounded
criticisms by some individuals who appear to adhere to the
"carbohydrates drive insulin which drives fat storage" mantra.  However,
this thinking is an example of cognitive miserliness, and I will address some of the comments of these critics here.

Some people have argued that my series on insulin only applies to
healthy people and not people with glucose intolerance, obese people, or
diabetics.  I briefly explained how this is not true here, but either these critics did not read that section of the article or ignored it.  To elaborate, some of the research I cited on protein and insulin secretion showed protein to be more insulinemic in obese people than lean people, yet we know that high protein intakes have been shown to be beneficial to helping obese people lose weight.  Obviously stimulation of insulin secretion is not a problem here.  Also, protein and carbohydrate tend to have a synergistic effect on insulin secretion when consumed together, creating a greater insulin response than when either one is consumed alone.  Yet, we know that a high protein, moderate-to-high carbohydrate, low-fat diet has been shown to be beneficial for weight loss.
 We would expect such a diet to cause significant postprandial insulin
secretion based on the combination of protein and carbohydrate, yet the
diet causes significant weight loss.  Why?  Because of the effects of
protein on satiety, resulting in people simply eating less.  Therefore,
it comes down to a matter of energy balance.  The postprandial insulin
secretion is irrelevant...insulin cannot trump the laws of physics.


To further illustrate how all of this data applies to all individuals
and not just healthy people, let's take a look at the effects of dairy
on insulin.  I
wrote extensively about how dairy products can be just as insulinemic,
if not more insulinemic, than high carbohydrate foods, including the
dreaded white bread.  If augmented postprandial insulin secretion is
a problem for obese people, type 2 diabetics, or glucose intolerant
people, then we would expect dairy to be a problem for these populations
as well.  However, we know that they are not.  Diets high in dairy do not impair weight loss or blood sugar control in overweight people, and they improve insulin sensitivity and attenuate weight gain in animal models.  We also know that a high intake of dairy products is associated with a lower risk of metabolic syndrome and type 2 diabetes.
 Thus, it is obvious that augmented postprandial insulin secretion is
not the problem that some have made it out to be, even for people with
health issues.


Some critics claimed that it is the combination of high postprandial
insulin and high postprandial glucose that is the problem, not insulin
itself.  However, if this were truly the issue, then we would still
expect dairy to increase risk of weight and fat gain, since most people
consume dairy along with foods that elevate glucose (most people do not
consume dairy alone).  Yet, we know from a large number of studies that dairy does not increase weight gain risk, and decreases weight gain in animals.
 This is despite the fact that dairy is being consumed with
glucose-elevating foods.  The problem here is that the critics are
taking an overly reductionistic view of insulin and body fat deposition.
 Since insulin enhances glucose uptake of fat cells, and since insulin
also inhibits lipolysis, these critics are concluding that the
combination of high insulin and high glucose will cause fat gain.
 However, this view is incorrect.  In fact, dairy products will increase the uptake of glucose into fat cells, yet result in less fat and weight gain.  Thus, things are not as simple as the critics make them out to be.


One critic pointed out how I had discussed insulin's inhibition of
lipolysis, and then insinuated that this is how insulin leads to fat
gain.  Yet, on the same token, this same critic stated that it was the
high insulin and high glucose that is the problem, not high insulin
itself.  This was an inconsistency in this critic's position.  Obviously
the latter assertion is incorrect based on what I discussed in the
previous paragraph.  Regarding the former insinuation, it again is an
overly reductionistic view of insulin in the body.  Yes, insulin
inhibits lipolysis, but it only takes small elevations in insulin to do
this, and this does not address what happens over a 24-hour period.  It
also does not address all of the other dozens of hormones and other
factors simultaneously interacting on fat tissue.  Not only that, but if
the former insinuation were true, then we would again expect dairy
products to promote fat gain in animals and humans, yet we know that
they do not.


Some critics claimed that the protein/insulin secretion studies I cited in this article mainly involved liquid and not solid foods.  However, only some of the studies involved liquids.  Other studies (such as this one and this one) involved solid foods.


Some critics created a straw man and stated that I was claiming that protein is just as insulinemic as carbohydrate.  In fact, one critic said, "I can't believe Krieger is here trying to say that protein causes more insulin release than sugar!"  However, I only said that protein can
be just as insulinemic as carbohydrate (can is the key word here).
 Certainly, when you average across all foods, carbohydrate produces the
greatest insulin responses, and protein comes in second.  However, when
you start looking at individual foods, some protein sources can produce
similar insulin responses to some carbohydrate foods (even some
carbohydrate foods that create rapid rises in blood glucose).  And this
is not to mention the synergistic effect that protein and carbohydrate
can have on insulin secretion when consumed together.  Yet, studies that
have combined the two have shown large amounts of weight and fat loss.


One particular critic that I saw created a huge load of straw men and other fallacies.   First, this individual said, "Unlike
what Krieger says, insulin release actually first starts when you start
to put the food in your mouth...It is wrong to say that insulin
secretion starts only after the glucose is already in the blood." This individual is referring to cephalic phase insulin secretion,
and the statement is a straw man because I never claimed that cephalic
phase insulin secretion does not exist or that insulin secretion starts
only after glucose is already in the blood.  This individual then said
that nobody claims that high carbohydrate diets lead to chronically high
insulin levels.  I am not sure what this critic has been reading as I
see this claim made quite often from numerous individuals all over the
internet, including low carbohydrate diet gurus.  Perhaps this
individual has never said this, but that does not mean that others have
not.   This individual went on to make the claim that "Our argument is high insulin tends to drive fat storage."
 Again, if the statement were true, then dairy products should promote
fat storage, yet they do not.  Also, if that statement were true, then
that would mean that insulin levels should predict future weight gain.
 However, the
vast majority of prospective studies have failed to show a relationship
between either basal or postprandial insulin levels and future weight
gain; in fact, some studies have shown higher insulin levels to be predictive of less weight gain in overweight people.  Also, insulin levels are not predictive of weight loss.  Thus, the concept that high insulin drives fat storage is a concept not supported by the scientific data.


This individual then created a strawman out of my statement of how consuming 5000 calories worth of olive oil or table sugar is not very palatable,
and tried to contradict that by claiming that it's difficult to eat
5000 calories worth of steak but easy to eat 5000 calories worth of cake
or similar high carbohydrate foods.  Well, it's not easy to consume
5000 calories worth of steak because of the high protein content and
because that would take a lot of chewing that would eventually get old.
 I could easily dump 5000 calories of a full-fat dressing (Caesar salad,
anyone?) and it would not be difficult at all to consume that amount.
 In fact, I would find that easier to consume (due to the energy
density) then 5000 calories worth of cake.  Along these lines, in the weight loss program for which I used to do research,
one client was not losing weight and swore she was following the
program.  Her husband eventually ratted her out and told the dietitian
that she was consuming over 8 tablespoons of peanut butter per day.
 That's close to 1,000 calories per day that she was not reporting.
 Eight tablespoons is a very easy way to quickly consume a large amount
of calories, despite the fact that peanut butter is mostly fat and low
in carbohydrate.  The ease of consuming a large number of calories of a
particular food depends much more on the palatability, the protein
content, the food form (solid versus liquid), the water content, the
energy density, and the fiber content, then it does on the carbohydrate
content.


This individual then stated that insulin "makes you hungry because it leads to insulin swings and hypoglycemia a few hours later."
 Well, insulin does not lead to insulin swings.  I think that this
person was referring to carbohydrate.  There is often the claim that
high glycemic carbohydrate will cause a rapid rise in blood sugar and
insulin, followed by a crash which will induce hunger.  However, this
concept is not fully supported by the scientific data.  High glycemic
foods do not necessarily have low satiating power; in fact, one
study that rated foods on their ability to create satiety found that
some high glycemic carbohydrate foods, such as potatoes and white rice,
were among the most satiating of all of the foods tested.  Another study found
a weak relationship between the glycemic response of a breakfast and
energy intake at lunch, but no relationship between the insulin response
to the meal and energy intake at lunch.  In a meta-analysis of the relationship between blood glucose responses and appetite, no relationship was observed, and higher insulin levels were actually associated with decreased hunger.


As I stated in a previous blog post, human appetite control is highly complicated.
 Things are not as simple as "glucose goes up, insulin goes up, glucose
then crashes and hunger increases."  Even if the latter were true
(which it is not given the scientific data), most people do not consume
high glycemic carbohydrates by themselves.  They generally consume them
with other foods, which dramatically changes the blood sugar and insulin
responses.


This critic goes on to say, "Type 2 diabetics are still often
hungry even though their blood sugars are constantly high. If insulin is
so good at satiating, then why do these diabetics still feel hungry?"
 Type 2 diabetics have insulin resistance in the brain, which disrupts
insulin's ability to signal the brain to reduce food intake.


This critic also states that nobody said that "carbohydrates are singularly responsible for driving insulin."  Actually Gary Taubes said it in his book, word for word.  She goes onto say that, regarding one particular study I referenced,
I claimed that 75 grams of carbohydrate was "low carbohydrate."  I
never made that claim; the study labeled it as such.  I clearly
addressed this with this paragraph:

Some people might argue that the “low-carb” condition
wasn’t really low carb because it had 75 grams of carbohydrate.  But
that’s not the point.  The point is that the high-carb condition had
nearly TWICE as much carbohydrate, along with a HIGHER glucose response,
yet insulin secretion was slightly LOWER.  The protein was just as
powerful at stimulating insulin as the carbohydrate.

This critic then goes on to my comments regarding how some in the
low-carbohydrate community claim that the insulin response to protein is
due to the gluconeogenesis from the protein.  She states, "Then he
says that 'some' might say it is due to gluconeogenesis. Really? WHo
would need to argue that when their drink has CARBOHYDRATES in it
already!" This critic completely missed the point, and needs to
look at the graphs of the blood insulin and glucose responses.  First,
the carbohydrate in the drink was quite low (only 11 grams) and did not
cause much change in blood glucose.  However, there was a very large
insulin response.  This means that the insulin response was not due to the blood glucose response.
 This completely contradicts the claims of some low-carbohydrate
advocates that the insulin response from protein is due to the protein
being converted to glucose, which would then drive up insulin.  I then
supported this further by citing research showing that amino acids directly stimulate the pancreas to produce insulin.


This individual goes on to state, "The weirder thing is this
study actually shows what we argue, ie that obese people have higher
insulin response to the same meal compared to nonobese. This will be
true of both protein AND carbs but he only talks about protein here.
Thus supporting our argument that insulin drives weight gain."  This individual is committing the cum hoc, ergo propter hoc ("with this, therefore because of this") fallacy.
 The fact that obese people present with high levels of insulin does
not mean that high insulin causes the obesity; they are simply
correlated.  In fact, not all obese people have high insulin levels.
 High insulin is not the driver of obesity; rather, it is the result of
obesity and the insulin resistance that often accompanies it.  Insulin
resistance is causing the high insulin in obese people (the high insulin
is the body's way to compensate for insulin resistance).


I will continue to address other criticisms that I have seen next week, along with continuing last week's article on how insulin regulates blood sugar.

Insulin: An Undeserved Bad Reputation, Part 4: The Biggest Insulin Myth of Them All » Weightology Weekly

Insulin: An Undeserved Bad Reputation, Part 4: The Biggest Insulin Myth of Them All » Weightology Weekly

In part 1, part 2, and part 3
of this series, you learned how there are a lot of misconceptions on
how insulin works in the body, and how it has been unfairly blamed for
weight and fat gain in our society.  In this article, I am going to
dismantle one of the biggest insulin myths of them all...a myth that has
been perpetuated in textbooks and is still taught in college
classrooms, despite the fact it was shown to be wrong over 25 years ago.

Insulin Is Not Required for Cells To Take Up Glucose


Are you surprised by the heading above?  Many people think that your
cells need insulin to take sugar out of the blood.  One of the pieces of
evidence that is offered for this is the type I diabetic.  When a type I
diabetic has no insulin, blood sugar skyrockets.  This is supposedly
because sugar can't get into cells.


However, the above scenario is not what happens in a type I diabetic
that has been taken off of insulin.  Sugar can get into the cells just
fine.  There's actually something else going on.  A review paper published in the Journal of Anasthesia
thoroughly describes how insulin has been misunderstood in its role in
blood sugar regulation, and I will summarize this paper here, along with
some of my own comments.


A Man Ahead of His Time


In 1916, Sir Edward Schafer, a professor of physiology, published a book called The Endocrine Organs.  In this book, he hypothesized the existence of what we now call insulin:

The results of  pancreas extirpation and pancreas
grafting are best explained by supposing that the islet tissue produce
an Autacoid which passes into the blood stream and effects carbohydrate
metabolism and carbohydrate storage in such a manner that there is no
undue accumulation of glucose in the blood.  Provisionally it will be
convenient to refer to this hypothetical substance as insuline.

Insulin would go onto be discovered 8 years later.  Schafer also
hypothesized that insulin was created from an inactive precursor:

It must however be stated that it has yet to be
determined whether the active substance is produced as such in the
pancreas or whether it exists there as pro-insuline which becomes
elsewhere converted into an active autacoid.

Pro-insulin was discovered nearly 50 years later.  Schafer was truly a man ahead of his time.


Schafer avoided using the term "hormone" to describe insulin. 
Instead, he used the terms "autacoid" and "chalone."  An autacoid was a
substance with excitatory action, meaning it stimulated things to happen
in your body.  An autacoid can be thought of as similar to the gas
pedal in your car; you step on the pedal and it stimulates your car to
go faster.  A chalone was a substance with inhibitory action; it slows
things down in your body.  A chalone can be thought of as similar to the
brake in your car.  Schafer correctly hypothesized that insulin acted
as both an autacoid and chalone in your body.  He also considered that
insulin acted as much more of a chalone than an autacoid in your body. 
In other words, he felt that insulin's inhibitory functions were much
more important than its excitatory or stimulatory functions.  He would
be proven correct many years later.


The Black Age of Endocrinology


However, before Schafer was proven correct, the "Black Age of
Endocrinology" ensued.  This was the time period between 1950 and 1980,
where scientists extrapolated beyond their discoveries.  They took in vitro animal data (research performed in a test tube or culture), and then assumed that the same thing happens in humans in vivo (inside the body).  In fact, one of the reasons I am so highly critical of Gary Taubes and his Good Calories, Bad Calories book
is that he relies heavily on research from this period, despite the
fact that much of what was thought then has either been overturned by
better research, or at least significantly altered.  Taubes even stated
around the 31 minute mark in this interview
that he doesn't pay attention to modern research because "all of this
should have been obvious decades ago."  This is a surprising stance for a
science writer; I would think that he would understand that conclusions in science are always tentative. 
This is particularly true in the nutritional and physiological
sciences, where advances in measurement techniques have allowed us to
measure and discover things that we could not measure before; this has
overturned or modified many hypotheses and thoughts over the years.  But
I digress.


The Black Age of Endocrinology is what led to the now mistaken belief
that insulin is needed for your cells to take up glucose.  Experiments
in the 1950s showed that insulin could stimulate bits of rat muscle and
fat to take up glucose.  This data was extrapolated to humans, and it
was then incorrectly hypothesized that a lack of insulin results in
glucose not being able to get inside your cells, and thus blood glucose
climbs to dangerous levels.  This erroneous thinking has now been taught
in textbooks and college classes all over the world for many years,
resulting in dogma.  Unfortunately, it is very difficult to overcome
dogma, and even though this concept of insulin was shown to be wrong in
the 1970's, it still continues to be taught to this day.


Glucose Transport is Not Insulin Dependent


The erroneous hypothesis that insulin withdrawal results in high
blood glucose because "glucose can't get into cells" was based on the
assumption that insulin is required for cells to take up glucose, rather than insulin merely enhancing
glucose uptake.  What the scientists in the 1950s failed to note was
how tissues can take up considerable amounts of glucose even when
insulin is absent.


Glucose enters your cells via a family of transporters.  A primary
transporter in muscle and fat cells is known as GLUT-4.  Insulin
stimulates GLUT-4 to move from the interior of a cell to the cell
surface, where the glucose can then bind to the GLUT-4 transporter and
enter the cell.  However, there are plenty of glucose transporters on
the cell surface, even when there is no insulin.  In fact, there are
enough transporters on the cell surface to allow the cell to get enough
glucose to sustain its energy needs.  Thus, glucose transport into cells
is never truly dependent upon insulin.  Insulin enhances the uptake of
glucose into cells, but it is not required for it.  In fact, when you
knock out the insulin receptor in mice so that insulin cannot stimulate
glucose uptake into muscle or fat cells (yet you keep the insulin
receptor intact on other cells like brain and liver), the animals do not become diabetic and they have normal blood sugars.


What Really Happens in a Type I Diabetic


Metabolic tracer studies have allowed us to learn how insulin operates in humans in vivo. 
When you take a type I diabetic off insulin, blood glucose climbs
sharply.  However, it's not because glucose can't get into cells.  In
fact, glucose uptake into cells actually increases.  This is because the
concentration of glucose in the blood is so much higher than the
cellular concentration that glucose must move into the cells (remember,
there's already enough glucose transporters on the cell surface even if
there's no insulin).  So why does blood glucose climb so high?  Remember
that the amount of glucose in your blood is both a function of how much
glucose is entering the blood (the rate of appearance), as well as how much glucose is leaving the blood (the rate of disappearance). 
In a fasted diabetic without insulin, all of the glucose is coming from
the liver.  Remember that your liver helps maintain blood sugar levels
when you are fasted by releasing glucose; this glucose comes from both gluconeogenesis (the formation of glucose from non-carbohydrate sources, like protein) and glycogenolysis
(the breakdown of glycogen stored in your liver).  Insulin acts as a
brake (a chalone as Dr. Schafer described it) on these processes.  Thus,
when you do not have insulin, you have runaway gluconeogenesis and
glycogenolysis.  The high blood sugar in an uncontrolled diabetic is
thus caused by overproduction of glucose from the liver, not because
glucose can't get into cells.


In fact, since insulin is not present, many processes go forth at
high rates, completely unregulated.  Insulin normally inhibits the
production of ketones by your liver; without insulin to slow down ketone
production, ketones are produced at high rates, resulting in diabetic
ketoacidosis.  This is why hyperglycemia and ketoacidosis occur
simultaneously.  Without insulin, you also have accelerated proteolysis
(the breakdown of protein) and lipolysis (the breakdown of fat).  The
elevated amino acids in the blood provide further substrate for the
liver to continue to produce large amounts of glucose.  The elevated
fatty acids provide substrate for the liver to continue to produce large
amounts of ketones.


Thus, insulin is like a traffic cop or a stop light at an
intersection.  It helps slow down and control traffic.  Without a stop
light or traffic cop, cars go through the intersection uncontrolled and
you get traffic accidents.  Likewise, without insulin in the body,
gluconeogenesis, glycolysis, proteolysis, ketogenesis, and lipolysis all
proceed at high rates without anything to stop them.  The end result is
hyperglycemia, ketoacidosis, and eventually death.


When you inject insulin into an uncontrolled diabetic, you are now
providing a brake on all of the processes mentioned earlier.  You
inhibit production of glucose by the liver, so blood sugar falls. 
Because there is no longer hyperglycemia, glucose uptake into cells
actually decreases.  Lipolysis is inhibited, so free fatty acid
concentration falls to near zero.  Because there are no longer free
fatty acids to make ketones, ketone production slows down.  Proteolysis
is also inhibited.


Insulin...More of a Traffic Cop Than a Storage Hormone


Metabolic tracer studies have proven what Schafer had hypothesized
nearly a century ago...that insulin's main role in the body is
inhibitory rather than excitatory.  While insulin certainly does have
excitatory functions, it is not primarily a "storage hormone" that many
individuals claim that it is.  Insulin is not needed for your cells to
take up and store glucose.  Certainly, it enhances uptake, but there is a
big difference between enhancing uptake and being needed for uptake.


Of course, this research only tells us what happens when insulin
is present versus when it is not present.  What about the normal
situation of a healthy person, who ingests a meal and sees a rise in
blood glucose?  What is happening to bring glucose back to normal?  And
what happens in a type II diabetic in this situation?  Learn the answers to these questions by reading part 6 of the series.  Also click here to read part 5 where I address comments made by some of the critics of this series.


REFERENCE:  Sonksen, P., and Sonksen, J.  Insulin: understanding its action in health and disease.  British Journal of Anaesthesia.  85(1):69-79, 2000.

Insulin: An Undeserved Bad Reputation, Part 3…MOOOOO!!!! » Weightology Weekly

Insulin: An Undeserved Bad Reputation, Part 3…MOOOOO!!!! » Weightology Weekly

This article represents part 3 of a series on
how insulin has been unfairly demonized by many in the nutrition
field.  If you have yet to read the first few parts, you can read Part 1 here, and you can read Part 2 here. 
In this article, I will discuss how dairy products are among the most
insulinemic foods out there, yet do not promote fat or weight gain,
which pokes holes in the hypothesis that carbohydrates drive fat
accumulation through insulin secretion. 

Dairy Products Are Insulinemic Yet Don't Promote Weight Gain


One of the premises of individuals like Gary Taubes is that
carbohydrates stimulate fat accumulation by stimulating insulin
secretion.  I've already shown how this premise is flawed in the last
two parts of my series.  Namely, I
showed how protein also stimulates insulin secretion (sometimes as much
as carbohydrate) yet does not promote weight or fat gain.  I also showed how the drug exenatide restores rapid-phase insulin secretion in diabetics yet promotes weight loss.


If the carbohydrate/insulin hypothesis were true, then we would
predict that foods that are extremely insulinemic would be uniquely fat
promoting.  What many people do not realize is that dairy foods are
among the most insulinemic foods out there.  In fact, they create much
greater insulinemic responses than you would expect based on their
carbohydrate content.  Not only that, but lactose, the primary
carbohydrate in dairy foods, is actually low glycemic and produces slow
rises in blood sugar (lactose has a glycemic index of 46 compared to white bread which is 100).  In fact, the
glycemic index of many dairy products is quite low, with full-fat milk
at 39, skim milk at 37, ice cream at 51, and fruit yogurt at 41.


Despite the low blood sugar responses, dairy products create very large insulin responses.  For example, in one study,
dairy products created similar or greater insulin responses than white
bread, despite the fact that the blood sugar response for some of the
dairy products was 60% lower than the white bread.  In this study, the
researchers compared the glycemic and insulinemic responses between
white bread, a low gluten/lactose mixture, a high gluten/lactose
mixture, cod with added lactose, milk, whey protein with added lactose,
and cheese with added lactose.  All of the conditions contained 25 grams
of carbohydrate and 18.2 grams of protein, except for the white bread
and low gluten/lactose mixtures, which contained 25 grams of
carbohydrate and 2.8 grams of protein.  Thus, lactose was the
carbohydrate in all of the conditions except for white bread.


When you look at the insulin area-under-the-curve (AUC) for the
various conditions, you can see that the dairy products actually created
greater insulin responses than the white bread, despite having similar
amounts of carbohydrate:

Insulin response of dairy foods compared to white bread

It is obvious that it is not the lactose that is responsible for the
greater insulin response, because the gluten/lactose and cod/lactose
mixtures resulted in similar or lower insulin responses to white bread.


The blood sugar response was also not responsible for the greater
insulin response.  In fact, the blood sugar response was lower in all of
the conditions compared to the white bread, with the milk creating the
lowest blood sugar response yet 3rd highest insulin response:

Blood glucose response to dairy foods compared to white bread

The insulinogenic index, which relates the amount of insulin
secretion to the blood glucose response, was significantly higher in the
dairy products, indicating that the dairy products stimulated much
greater insulin secretion that you would expect based on the blood
glucose response:

Insulinogenic index of dairy products compared to white bread

This is not the only study to show the insulinemic effects of dairy products.  I showed in my previous article how whey protein, a dairy protein, created the highest insulin response compared to non-dairy proteins.  In a study on type 2 diabetics,
the inclusion of whey protein in a meal increased the insulin response
by 31-57%, while the blood glucose response was reduced by up to 21%.  In another study,
the addition of 400 mL of milk to a bread meal increased the insulin
response by 65%, despite the fact there was no change in the blood
glucose response.  In this same study, the addition of 200 or 400 mL of
milk to a spaghetti meal increased the insulin response by 300%; again,
there was no change in the blood glucose response.  In fact, drinking
milk with the spaghetti meal created an insulin response that was
similar to white bread.


Here's the results of another study showing the glycemic and insulinemic indexes of milk compared to white bread:





Why Does Dairy Stimulate So Much Damn Insulin?


It is clear that dairy products stimulate large amounts of insulin
secretion, as much or more than white bread.  One of the reasons dairy
products create large insulin responses is due to their amino acid
content.  In fact, the
postprandial insulin response from dairy products correlates with the
rise in branched chain amino acids leucine, valine, and isoleucine.  I already pointed out in part 1 of this series how leucine will directly stimulate your pancreas to produce insulin.


Another reason that dairy products stimulate so much insulin
secretion is their effects on a hormone called glucose-dependent
insulinotropic polypeptide (GIP).  Like GLP-1 which I wrote about in part 2 of this series, GIP is an incretin. 
This means that it is a hormone produced by your intestines that
stimulates insulin secretion.  Dairy products stimulate increased
production of GIP.  In the study I discussed earlier
which compared whey, milk, and cheese to white bread, whey and cheese
resulted in 21-67% greater GIP responses than white bread:

Glucose-dependent insulinotropic polypeptide (GIP) response to dairy foods compared to white bread

The above data illustrates one of the problems with the
carbohydrate/insulin hypothesis...it assumes that carbohydrate is the
primary stimulus of insulin secretion.  However, it is clear that amino
acids and incretins play significant roles in insulin secretion as
well.  And as I pointed out in part 1 of this series,
the blood sugar response of a food only explains 23% of the variation
in the insulin response.  Thus, a lot more goes into insulin secretion
than the blood sugar response from eating carbohydrate.


Dairy and Weight Gain/Loss


It is clear that dairy products are extremely insulinemic, moreso
than many high carbohydrate foods.  Thus, if the carbohydrate/insulin
hypothesis were true, then we would predict that a diet high in dairy
products should promote weight and fat gain.  However, studies fail to
show any relationship between dairy product intake and weight gain.  For
example, there is no relationship between intake of dairy products and BMI in Japanese women.  In U.S. men, there is no relationship between an increase in dairy consumption and long-term weight gain.  In perimenopausal women, high
intakes of dairy products are actually inversely associated with weight
gain (i.e, higher dairy product intakes are associated with less weight
gain).


While these are observational studies, the results from controlled
studies on animals and humans are similar.  In fact, animal studies show
less weight gain when they are fed dairy products.  In mice, yogurt supplementation results in less weight and fat gain than controls on isocaloric diets.  In another study, transgenic mice lost weight on energy restricted diets.  The mice were then allowed to eat ad libitum (i.e., as much as they felt like).  The mice fed dairy products regained less fat and weight during refeeding.  In a third study, the intake of dairy products, but not a calcium supplement, decreased weight gain and body fat in mice fed a high-fat diet.  In a fourth study, dairy protein attenuated fat gain in rodents fed a high-fat, high-sugar diet.  In a fifth study, a dairy diet attenuated weekly weight gain in Sprague-Dawley rats.


Of course, these are animal studies.  What about humans?  In one study,
low-fat dairy products did not promote weight gain, while high-fat
dairy products did.  Hmmm, could it be that the weight gain in this
study was simply caused by excess calories and not insulin?   In another study, increased intake of dairy products did not affect body composition.  In a third study, increased intake of dairy products did not impair weight loss.  In a one-year study, increased intake of dairy products did not affect changes in fat mass.  In a 6-month follow-up to this study, high dairy product intake predicted lower levels of fat mass.  In a 9-month study,
increased intake of dairy products did not affect weight maintenance,
but the high dairy group exhibited evidence of greater fat oxidation.


Why Am I Not Fat?


My own personal experience with dairy fits right in with the
science.  I consume a lot of dairy and have for many years.  I go
through 2-3 gallons of milk per week.  I also go through a lot of Greek
yogurt, cottage cheese, regular cheese, and whey protein.  I have some
type of dairy with just about every meal.   Thus, I have large amounts
of insulin flowing through my body pretty much all day.  If insulin was
truly the fat-promoting, weight-gaining hormone that some have made it
out to be, then I should be obese by now.  Yet, I am not...not even
close.


Not only that, but the people who think insulin makes you hungry,
that would imply that I should be starving all of the time with all of
the insulin that is flowing through my body all day.  Yet, I'm not.


Got Milk?  Got Insulin!


The evidence is overwhelming that dairy products do not promote
weight gain, and they actually inhibit weight gain in animal studies. 
This is despite the fact that dairy products produce very large insulin
responses, as much or greater than many high carbohydrate foods.  Thus,
it is clear from this article, as well as my previous articles, that the
carbohydrate/insulin hypothesis is incorrect.  Insulin is not the
criminal in the obesity epidemic; instead, it is an innocent bystander
that has been wrongly accused through guilt by association.


Click here to read part 4 of my series, where I address the misconception of how insulin regulates blood sugar.

Insulin: An Undeserved Bad Reputation, Part 2 » Weightology Weekly

Insulin: An Undeserved Bad Reputation, Part 2 » Weightology Weekly

In a previous issue of Weightology Weekly, I wrote about insulin and how it's been unfairly demonized by many in the nutrition field. 
This demonization has been based on a number of misconceptions
regarding insulin, its biological effects, and its secretion.  I want to
continue clarifying these misconceptions. 

MYTH:  Insulin Spikes are "Bad"


FACT:  Insulin Spikes Serve a Normal & Important Physiological Function


In my previous article,
I discussed how dietary protein can cause insulin spikes just like
dietary carbohydrate, and these spikes are not related to
gluconeogenesis from the protein (i.e., the protein being converted to
sugar).  I also showed how these spikes are partly responsible for the
suppression of appetite that is caused by dietary protein (due to
insulin's effects on your brain to inhibit appetite).


I want to expand on the importance of rapid insulin spikes due to
feeding, and how they are important in blood sugar regulation.  To do
this, we need to discuss the phases of insulin secretion.  Insulin
secretion from your pancreas comes in two phases.  The first phase
happens very quickly; your pancreas senses rising glucose, and insulin
is released within 1-2 minutes of this rise in blood sugar.  This
rapid-phase response is the result of your pancreas releasing stored
insulin.  It is typically over within 10 minutes.  This rapid-phase
response has been found to be impaired in people with impaired glucose tolerance
(people who have higher blood sugar responses to meals than normal, and
higher fasting levels of blood sugar, but who are not diabetic).  This
rapid-phase response is completely absent in people with type 2
diabetes.


There is a second phase that continues as long as glucose is
elevated.  This release of insulin is achieved by the release of stored
insulin, as well as the creation of new insulin (insulin is created from
a precursor called proinsulin).  When you infuse glucose into the blood
of healthy people and type 2 diabetics, you get insulin responses that
look like this:

Insulin Response to Intravenous Glucose Administration in Healthy People Versus Type 2 Diabetics

You can see that the diabetics completely lack the rapid phase response that is present in the healthy individuals.


There is a drug called exenatide (Byetta),  which has been found to restore this rapid phase insulin response in diabetics:

Insulin
responses of type2 diabetics and healthy individuals, who have been
administered glucose intravenously. Circles represent the insulin
response of the type 2 diabetics when given a placebo. Squares represent
the insulin response of the diabetics when given exenatide. You can see
that exenatide restores the rapid phase insulin response. Black circles
represent the insulin response of healthy individuals.

This restoration of the rapid phase insulin response improves blood sugar regulation in diabetics:

Blood
sugar response to a meal in type 2 diabetics. Circles represent
subjects on a placebo. Dark triangles and circles represent subjects on
exenatide. You can see that blood sugar remained steady in the subjects
on exenatide, but gradually increased in the subjects on the placebo.

 You can see in the above chart that blood sugar remained consistent
in response to a meal in the subjects on exenatide, but it increased
over time in the subjects on the placebo.


Many people like to blame obesity and weight gain on insulin, but
exenatide, which restores insulin spikes in type 2 diabetics, causes
weight loss:

Effects of exenatide (Byetta) on body weight

Part of this weight loss is due to an improvement in satiety. 
Exenatide is a drug that mimics the effects of a hormone called
glucagon-like peptide-1 (GLP-1).  GLP-1 is an intestinal
insulin-stimulating hormone (known as an incretin).  GLP-1 potentiates
insulin secretion, enhances the synthesis of insulin, upregulates
insulin gene expression, and inhibits glucagon (insulin's opposing
hormone) secretion.  Yet Exenatide, which mimics GLP-1 and helps
stimulate insulin secretion, causes weight loss.


The fact is that rapid insulin spikes in and of themselves are not a
bad thing.  Protein causes rapid insulin spikes, yet protein reduces
appetite and helps with weight loss.  GLP-1 and drugs like exenatide
contribute to insulin spikes, yet they reduce appetite and cause weight
loss.  The problem is that people confuse insulin spikes and blood
glucose spikes.  It is well established that rapid rises and falls in blood glucose can contribute to hunger. 
Because rapid rises in blood glucose also cause rapid rises in insulin,
people end up blaming insulin (and the effects of high glycemic
carbohydrates on insulin) for the problem. 


MYTH:  Since diabetics who inject insulin gain weight, this means that insulin is the reason for weight gain in non-diabetics


FACT:  Amylin is co-secreted with insulin in non-diabetics; amylin has appetite suppressant and lipolytic effects


I would like to thank Dr. Stephan Guyenet
for this information.  I had known about amylin but hadn't looked into
it in any great detail.  Amylin is a hormone that is secreted by your
pancreas at the same time as insulin.  Amylin decreases appetite, and also stimulates lipolysis (the breakdown of fat into fatty acids).


Type 1 diabetics do not produce amylin, and amylin secretion is impaired in type 2 diabetics.  Pramlintide, a drug that mimics the effects of amylin, has been found to produce weight loss in diabetics.


This information demonstrates that the effects of insulin injection
in a diabetic cannot be compared to the effects of physiological changes
in insulin in a non-diabetic, yet many people erroneously make this
comparison as if they are similar.


MYTH:  Lowering Insulin Will Improve Appetite Regulation


FACT:  Insulin Is One of the Many Hormones Critical to Satiety


I already most addressed this myth in my previous article on insulin,
showing how protein stimulated insulin secretion and helped reduce
appetite, and also showing how insulin injection into the brain reduces
appetite.  I again want to thank Dr. Guyenet for this information, but when you knock out the insulin receptors of a mouse's brain, the mouse will overeat and develop obesity.


MYTH:  All of this information only applies to healthy people


FACT:  The information applies to obesity and diabetes


On other forums, I saw people comment on my previous article and
claim that the information I provided only applied to healthy people,
and not diabetics or obese individuals.  They continued to believe that
treating diabetes and obese individuals was all about insulin control. 
Nothing could be further from the truth.  Not only is this evident from
information mentioned earlier in this article (such as how exenatide
restores insulin spikes and improves blood sugar control and body weight
in diabetics), but it is also evident from the fact that high protein
diets have been found to help both diabetics and obese individuals,
despite the fact that protein is a powerful stimulus of insulin
secretion.


As I mentioned earlier, people seem to confuse blood glucose control
and insulin control.  It is the management of blood glucose itself that
is partly responsible for the health benefits of low-glycemic
carbohydrates, or reducing carbohydrates, or increasing protein intake,
or consuming dietary fiber, or consuming fruits and vegetables, or
consuming whole foods over processed foods.  It is not the control of
insulin; the control of insulin ends up being a byproduct of these other
behaviors through improvements in insulin sensitivity (how responsive
your cells are to insulin) and reductions in blood sugar swings.


Remember, insulin is not the bad guy.  Click here to read part 3 of this series, where I discuss how dairy products are extremely insulinemic, yet do not promote weight gain.

Insulin…an Undeserved Bad Reputation » Weightology Weekly

Insulin…an Undeserved Bad Reputation » Weightology Weekly

I feel sorry for insulin.  Insulin has been
bullied and beaten up.  It has been cast as an evil hormone that should
be shunned.  However, insulin doesn't deserve the treatment it has
received. 

Insulin: A Primer


Insulin is a hormone that regulates the levels of sugar in your
blood.  When you eat a meal, the carbohydrate in the meal is broken down
into glucose (a sugar used as energy by your cells).  The glucose
enters your blood.  Your pancreas senses the rising glucose and releases
insulin.  Insulin allows the glucose to enter your liver, muscle, and
fat cells.  Once your blood glucose starts to come back down, insulin
levels come back down too.  This cycle happens throughout the day.  You
eat a meal, glucose goes up, insulin goes up, glucose goes down, and
insulin goes down.  Insulin levels are typically lowest in the early
morning since it's usually been at least 8 hours after your last meal.


Insulin doesn't just regulate blood sugar.  It has other effects as well.  For example, it stimulates your muscles to build new protein (a process called protein synthesis).  It also inhibits lipolysis (the breakdown of fat) and stimulates lipogenesis (the creation of fat).


It is the latter effect by which insulin has gotten its bad
reputation.  Because carbohydrate stimulates your body to release
insulin, it has caused some people to argue that a diet high in
carbohydrate will cause you to gain fat.  Their reasoning, in a
nutshell, goes like this:


High Carbohydrate Diet -> High Insulin -> Increased
Lipogenesis/Decreased Lipolysis -> Increased Body Fat -> Obesity


Using this same logic, they argue that a low carbohydrate diet is
best for fat loss, because insulin levels are kept low.  Their logic
chain goes something like this:


Low Carbohydrate Diet -> Low Insulin -> Decreased Lipogenesis/Increased Lipolysis -> Decreased Body Fat


However, this logic is based on many myths.  Let's look at many of the myths surrounding insulin.


MYTH:A High Carbohydrate Diet Leads to Chronically High Insulin Levels


FACT:Insulin Is Only Elevated During the Time After a Meal In Healthy Individuals


One misconception regarding a high carbohydrate intake is that it
will lead to chronically high insulin levels, meaning you will gain fat
because lipogenesis will constantly exceed lipolysis (remember that fat
gain can only occur if the rate of lipogenesis exceeds the rate of
lipolysis).  However, in healthy people, insulin only goes up in
response to meals.  This means that lipogenesis will only exceed
lipolysis during the hours after a meal (known as the postprandial period). 
During times when you are fasting (such as extended times between
meals, or when you are asleep), lipolysis will exceed lipogenesis
(meaning you are burning fat).  Over a 24-hour period, it will all
balance out (assuming your are not consuming more calories than you are
expending), meaning you do not gain weight.  Here's a graph showing how
this works:

After
meals, fat is deposited with the help of insulin. However, between
meals and during sleep, fat is lost. Fat balance will be zero over a
24-hour period if energy intake matches energy expenditure.

This is just a rough chart that I made, but the green area represents
the lipogenesis occuring in response to a meal.  The blue area
represents lipolysis occuring in response to fasting between meals and
during sleep.  Over a 24-hour period, these will be balanced assuming
you are not consuming more calories than you expend.  This is true even
if carbohydrate intake is high.  In fact, there are populations that
consume high carbohydrate diets and do not have high obesity rates, such
as the traditional diet of the Okinawans.  Also, if energy intake is lower than energy expenditure, a high carbohydrate diet will result in weight loss just as any other diet.


MYTH:  Carbohydrate Drives Insulin, Which Drives Fat Storage


FACT:  Your Body Can Synthesize and Store Fat Even When Insulin Is Low


One of the biggest misconceptions regarding insulin is that it's
needed for fat storage.  It isn't.  Your body has ways to store and
retain fat even when insulin is low.  For example, there is an enzyme in
your fat cells called hormone-sensitive lipase (HSL).  HSL helps break
down fat.  Insulin suppresses the activity of HSL, and thus suppresses
the breakdown of fat.  This has caused people to point fingers at
carbohydrate for causing fat gain.


However, fat will also suppress HSL even when insulin levels are low. 
This means you will be unable to lose fat even when carbohydrate intake
is low, if you are overeating on calories.  If you ate no carbohydrate
but 5,000 calories of fat, you would still be unable to lose fat even
though insulin would not be elevated.  This would be because the high
fat intake would suppress HSL.  This also means that, if you're on a low
carbohydrate diet, you still need to eat less calories than you expend
to lose weight.


Now, some people might say, "Just try and consume 5000 calories of
olive oil and see how far you get."  Well, 5000 calories of olive oil
isn't very palatable so of course I won't get very far.  I wouldn't get
very far consuming 5,000 calories of pure table sugar either.


MYTH:  Insulin Makes You Hungry


FACT:  Insulin Suppresses Appetite


It is a well known fact that insulin acutely suppresses appetite.  This has been demonstrated in dozens and dozens of experiments.  This will be important when we talk about the next misconception...


MYTH:  Carbohydrate Is Singularly Responsible for Driving Insulin


FACT:  Protein Is a Potent Stimulator of Insulin Too


This is probably the biggest misconception that is out there. 
Carbohydrates get a bad rap because of their effect on insulin, but
protein stimulates insulin secretion as well.  In fact, it can be just
as potent of a stimulus for insulin as carbohydrate.  One recent study compared the effects of two different meals on insulin. 
One meal contained 21 grams of protein and 125 grams of carbohydrate. 
The other meal contained 75 grams of protein and 75 grams of
carbohydrate.  Both meals contained 675 calories.  Here is a chart of
the insulin response:

Comparison of insulin response between low protein, high carb meal and high protein, low carb meal

Now here's a chart of the blood sugar response:

Comparison of blood sugar response to low protein, high carb meal and high protein, low carb meal

You can see that, despite the fact that the blood sugar response was
much higher in the meal with more carbohydrate, the insulin response
wasn't higher.  In fact, the insulin response was somewhat higher after
the high protein meal, although this wasn't statistically significant.


Some people might argue that the "low-carb" condition wasn't really
low carb because it had 75 grams of carbohydrate.  But that's not the
point.  The point is that the high-carb condition had nearly TWICE as
much carbohydrate, along with a HIGHER glucose response, yet insulin
secretion was slightly LOWER.  The protein was just as powerful at
stimulating insulin as the carbohydrate.


I can also hear arguments coming like, "Yeah, but the insulin
response is longer and more drawn out with protein."  That wasn't true
in this study either.

Insulin response to high protein and high carb meals

You can see in the chart that there was a trend for insulin to peak
faster with the high protein condition, with a mean response of 45 uU/mL
at 20 minutes after the meal, versus around 30 uU/mL in the high carb
condition.


This tendency for a higher insulin response was associated with a
tendency towards more appetite suppression.  The subjects had a tendency
towards less hunger and more fullness after the high protein meal:

Comparison of low protein, high carb and high protein, low carb meals and their effects on hunger and fullness

Here's the results of another study
that compared the effects of 4 different types of protein on the
insulin response to a meal.   This study was interesting because they
made milkshakes out of the different proteins (tuna shakes???? 
YUCK!!!!!  Of course some people may remember the tuna shake recipes
from the misc.fitness.weights
days).  The shakes contained only 11 grams of carbohydrate, and 51
grams of protein.  Here's the insulin response to the different shakes:

Insulin Response to 4 Different Proteins

You can see that all of these proteins produced an insulin response,
despite the fact that the carbohydrate in the shake was low.  There was
also different insulin responses between the proteins, with whey
producing the highest insulin response.


Now, some might argue that the response is due to gluconeogenesis
(a process by which your liver converts protein to glucose).  The
thought is that the protein will be converted to glucose, which will
then raise insulin levels.  As I mentioned earlier, people will claim
that this will result in a much slower, more drawn-out insulin response,
since it takes time for your liver to turn protein into glucose. 
However, that's not the case, because the insulin response was rapid,
peaking within 30 minutes and coming back down quickly at 60 minutes:

Insulin response to different types of protein

This rapid insulin response was not due to changes in blood glucose. 
In fact, whey protein, which caused the greatest insulin response,
caused a drop in blood glucose:

Glucose response to different types of protein

The insulin response was associated with appetite suppression.  In
fact, the whey protein, which had the highest insulin response, caused
the greatest suppression of appetite.  Here's a chart showing the
calorie intake of the subjects when they ate lunch 4 hours after
drinking the shake:

Calorie intake at a lunch consumed 4 hours after consuming various protein

The subjects ate nearly 150 calories less at lunch when they had whey
protein, which also caused the greatest insulin response.  In fact,
there was an extremely strong inverse correlation between insulin and
food intake (a correlation of -0.93).


Here's data from another study
that looked at the insulin response to a meal that contained 485
calories, 102 grams of protein, 18 grams of carbohydrate, and almost no
fat:

Insulin response to a high protein, low carb meal in lean and obese people

You can see that the insulin response was exaggerated in the obese
subjects, probably due to insulin resistance.  Here's a chart of the
blood glucose response.  You can see there was no relationship between
the glucose response and insulin, which was similar to the study
discussed earlier.

Blood glucose response in response to a high protein, low carb meal in lean and obese

The fact is that protein is a potent stimulator of insulin secretion,
and this insulin secretion is not related to changes in blood sugar or
gluconeogenesis from the protein.  In fact, one study found beef to stimulate just as much insulin secretion as brown rice. 
The blood sugar response of 38 different foods could only explain 23%
of the variability in insulin secretion in this study.  Thus, there's a
lot more that's behind insulin secretion than just carbohydrate.


So how can protein cause rapid rises in insulin, as shown in the whey
protein study earlier?  Amino acids (the building blocks of protein)
can directly stimulate your pancreas to produce insulin, without having to be converted to glucose first.  For example, the amino acid leucine directly stimulates pancreas cells to produce insulin, and there's a direct dose-response relationship (i.e., the more leucine, the more insulin is produced).


Some might say, "Well, sure, protein causes insulin secretion, but
this won't suppress fat-burning because it also causes glucagon
secretion, which counteracts insulin's effects."  I mentioned earlier
how insulin will suppress lipolysis.  Well, some people think that
glucagon increases lipolysis to cancel this out.


The thought that glucagon increases lipolysis is based on 3 things:  the fact that human fat tissue has glucagon receptors, the fact that glucagon increases lipolysis in animals, and the fact that glucagon has been shown to increase lipolysis in human fat cells in vitro (in a cell culture).  However, what happens in vitro isn't necessarily what happens in vivo (in your body).  We have a case here where newer data has overturned old thinking.  Research using modern techniques has shown that glucagon does not increase lipolysis in humans.  Other research using the same techniques has shown similar results.  I will also note that this research failed to find any lipolytic effect in vitro.


It should be remembered why glucagon is released in response to
protein in the first place.  Since protein stimulates insulin secretion,
it would cause a rapid drop in blood glucose if no carbohydrate is
consumed with the protein.   Glucagon prevents this rapid drop in blood
sugar by stimulating the liver to produce glucose.


Insulin:  Not Such a Villain After All


The fact is that insulin is not this terrible, fat-producing hormone
that must be kept as low as possible.  It is an important hormone for
appetite and blood sugar regulation.  In fact, if you truly wanted to
keep insulin as low as possible, then you wouldn't eat a high protein
diet...you would eat a low protein, low carbohydrate, high fat diet. 
However, I don't see anybody recommending that.


I'm sure some are having some cognitive dissonance reading this
article right now.  I know because I experienced the same disbelief
years ago when I first discovered this paper
and how protein caused large insulin responses.  At the time, I had the
same belief that others have...that insulin had to be kept under
control and as low as possible, and that spikes in insulin were a bad
thing.  I had difficulty reconciling that study and my beliefs regarding
insulin.  However, as time went on, and as I read more research, I
learned that my beliefs regarding insulin were simply wrong.


Now, you may be wondering why refined carbohydrates can be a
problem.  Many people think it's due to the rapid spikes in insulin. 
However, it's obviously not the insulin, because protein can cause rapid
spikes in insulin as well.  One problem with refined carbohydrate is a
problem of energy density.  With refined carbohydrate, it is easier to
pack a lot of calories into a small package.  Not only that, but foods
with high energy density are often not as satiating as foods with low
energy density.  In fact, when it comes to high-carbohydrate foods, energy density is a strong predictor of a food's ability to create satiety (i.e.,
low-energy density foods create more satiety).  There are other issues
with refined carbohydrate as well that are beyond the scope of this
article.


The bottom line is that insulin doesn't deserve the bad reputation
it's been given.  It's one of the main reasons why protein helps reduce
hunger.  You will get insulin spikes even on a low-carb, high-protein
diet.  Rather than worrying about insulin, you should worry about
whatever diet works the best for you in regards to satiety and
sustainability.  As mentioned in last week's issue of Weightology Weekly,
individual responses to particular diets are highly variable and what
works for one person will not necessarily work for another.  I will be
writing a post in the future on the need for individualized approaches
to nutrition.


Click here to read part 2 of this series on insulin.