is written to get you motivated enough to do something as a parent or
community leader. The big question: Who's to blame for our current childhood
obesity and type 2 diabetes epidemic? Depends on whom you ask. The Institute
of Medicine says it's an interaction between genetics and environment. Well,
our genetics hasn't changed in 30 years, but our environment has. The body
mass index distribution curve shows that all segments of the population are
increasing in weight, so whatever's happening is happening to everybody. The
U.S. Government calls it a matter of "personal responsibility." How does the
2-year-old population, who is witnessing the greatest increase in prevalence
of obesity, accept personal responsibility? The Centers for Disease Control
and Prevention says obesity results from an energy imbalance, by eating too
many calories and not getting enough physical activity. Big Food says it's a
lack of activity, the TV industry says it's the diet. The Atkins people say
it's too much carbohydrate, the Ornish people say it's too much fat. The
juice people say it's the soda, the soda people say it's the juice. The
schools say it's the parents, the parents say it's the schools. How are we
going to fix this, when no one will accept responsibility? If you want to
just blame American apathy and laxity, all you have to do is look at Japan,
China, and France, each of which has witnessed a doubling in the prevalence
of childhood obesity in the last 10 years, as well as the rise in prevalence
in developing countries in which malnutrition used to be rampant. In other
words, it's not Americans; it's humans.
So far, it is
just "guilt by association." The not-my-fault two-step has so far succeeded,
due to a lack of mechanism, which has allowed each interest group to
sidestep their responsibility. So what really has happened in the past 30
years to allow for this? And how did our physiology interact with our
environment to create this problem?
reason for this conundrum is our casual misinterpretation of the First Law
of Thermodynamics, which states: "The energy within a closed system remains
constant." In human terms, the First Law is usually interpreted as follows:
"If you eat it (energy intake), you better burn it (energy expenditure), or
you're going to store it (weight gain)."
another equally plausible interpretation of the First Law, which is stated
thus: "If you store it, and you expect to burn it, then you have to eat it."
In this interpretation, the behaviors of gluttony and sloth become secondary
to a pathological process of excess energy storage. Could this instead be
what's happening? What is making energy storage go haywire?
dysfunctional energy storage, we must first understand how our body normally
regulates energy balance. Our energy intake vs. expenditure is normally
regulated very tightly by the hormone leptin, which transmits the primary
controls to the brain for energy balance.
signal (1) reduces the appetite to decrease further food intake,
(2)increases thyroid hormone and energy expenditure, 3) innervating
skeletal muscles to increase energy, and 4) innervating white adipose
tissue to release fat. The magnitude of energy expenditure also increase
energy expenditure (eg, caffeine) increase quality of life.
causes the brain to reduce the activity of the vagus nerve. The Vagus
increases insulin secretion to increase calories into fat cells, and
increases adipose tissue insulin sensitivity to promote energy accumulation
in fat. So when leptin levels are high, the brain senses energy
sufficiency, and these vagal energy conserving and storing processes are
has a "personal leptin threshold," above which the brain interprets a state
of energy sufficiency and the high leptin state is characterized by low
appetite, normal physical activity, and feelings of well-being.
conditions of low leptin, such as in the "starvation response," the brain
would of decrease the body’s activity and feelings of well-being, and
increase vagal tone to increase appetite and insulin release (to store more
energy in adipose tissue). In the energy excess state, humans burn energy at
50 kcal/kg fat-free mass. However, in the starvation state, this is reduced
to 40 to 42 kcal/kg fat-free mass.
Obesity is the
same process in the brain as starvation. On first thought this sounds
ludicrous, but in fact, it actually makes a lot of sense. If you examine the
constitutional symptoms of obese and starved individuals, they are similar.
Both are associated with fatigue, malaise, lack of activity, inability to
motivate, and depression. The reason for this is the ability or inability
for the brain to transduce the leptin signal; in starvation because there is
inadequacy of leptin, and in obesity because there is resistance to leptin,
because it is obviously not doing its job. Furthermore, serum leptin
concentrations drop precipitously during periods of short-term fasting
(with-in 12 hours), declining faster than body fat stores, which would
account for the recidivism of obesity; the hypothalamus is seeing a
declining leptin signal similar to starvation, promoting increased energy
intake and decreased energy expenditure. Similarly, giving leptin to obese
leptin-resistant individuals is not effective.
So what is
leptin resistance? And what restores leptin sensitivity? So far, two
paradigms for improving leptin sensitivity have been noted.
loss. Rosenbaum employed a 10% weight loss paradigm to induce the
starvation response. In these individuals, leptin declined and energy
expenditure decreased. However, exogenous administration of leptin in
physiologic dosing to approximate the prestarvation leptin level resulted in
further weight and fat decrease, along with return of energy expenditure to
the prestarvation state. In other words, in the baseline state, subjects
were resistant to physiologic concentrations of leptin, while in the
weight-reduced state, they were responsive to the same concentrations of
exogenous leptin; thus, forced weight loss improved their leptin
children who became obese after brain damage from brain tumors, surgery, or
radiation, termed "hypothalamic obesity." Death of these neurons prevents
normal leptin signaling, resulting in an "organic leptin resistance," which
manifests as a never-ending starvation response and intractable obesity.
Hypothalamic obesity is classically unresponsive to diet, exercise, and most
pharmacologic manipulations. We treated patients with the somatostatin
analog and insulin suppressive agent octreotide. We were able to suppress
insulin, stabilize BMI, decrease caloric intake, increase spontaneous
physical activity, and improve quality of life commensurate with the degree
of insulin suppression. In other words, reduction in insulin reduced hunger,
fatigue, malaise, and sloth.
treated obese adults (without CNS lesions) with octreotide. We noted
significant and progressive BMI loss in about 20% of treated subjects.
Recall measurements of caloric intake demonstrated that these responders
reduced carbohydrate intake selectively, along with suppression of insulin,
while nonresponders did not. In the responders, leptin concentration dropped
by 50%, which of necessity should elicit the "starvation response;" despite
this, energy expenditure increased in these subjects. We also demonstrated
that insulin suppression by octreotide correlated with improved leptin
WHAT IS THE
MECHANISM OF LEPTIN RESISTANCE?
Rosenbaum through forced weight loss, improved leptin sensitivity as
measured by improved energy expenditure in response to leptin. Insulin
suppression using octreotide also improved leptin sensitivity, as measured
by declining leptin with improved energy expenditure, allowing for weight
loss and improved quality of life. Both paradigms share at their core a
reduction in insulin concentrations. The similarity of effect between these
two paradigms suggest that insulin may be one cause of leptin resistance.
Antagonizes Leptin Signaling
Although insulin and leptin bind to separate receptors in the brain, they
share the same signaling cascade. It is thought that when insulin levels at
the brain are high, then leptin cannot turn on its signaling cascade.
Advantage for insulin as an Endogenous Leptin Antagonist
Teleologically, what could be the biological advantage of insulin antagonism
of leptin action in obesity? Leptin is a necessary signal to the brain for
the initiation of high-energy processes, such as puberty and pregnancy. If
leptin signaling were not modulable, the weight accrual for reproductive
competency during puberty and pregnancy would be compromised. Therefore,
reversible antagonism of leptin action is in the best interest of our
survival. Since insulin causes energy deposition into fat, it makes sense
that it should be the central blocker of leptin as well. Indeed, both
puberty and pregnancy are hyperinsulinemic and insulin resistant states;
with requisite increases in insulin levels. In both, leptin levels increase
slowly, and then when adulthood is reached or post-partum, insulin levels
fall, weight stabilizes or is lost, and leptin returns back toward baseline.
However, in maladaptive conditions when insulin rises chronically, leptin
signaling continues to be impeded, the brain sees starvation, and obesity
WHERE DID THE
HYPERINSULINEMIA COME FROM?
At least three separate reasons for hyperinsulinemia in children can be
Genetics: children from certain racial and ethnic groups have
increased insulin dynamics even prior to the development of obesity, which
may predispose them to increased weight gain.
Epigenetics: the "fetal origins of adult disease" hypothesis states
that those born small- and large-for-gestational age at birth are prone to
developing obesity; both birth weight extremes are states of
hyperinsulinemia and insulin resistance, which may worsen beyond the
Our Western environment through three separate submechanisms.
Increased stress with increased cortisol secretion may lead to
insulin resistance. Indeed, television watching may in-crease stress levels,
increase food intake, foment insulin resistance (as in Cushing's syndrome)
and promote obesity.
The loss of daily physical activity due to lack of sidewalks,
automobile transport, and screen time (TV, computers, cell phones) foments
Finally, and most significantly, our current Western food environment
is highly insulinogenic, as demonstrated by its increased energy density,
high fat content, high glycemic index, increased fructose composition,
decreased fiber, and decreased dairy content." In particular, fructose (too
much) and fiber (not enough) appear to be cornerstones of the obesity
epidemic, through their effects on insulin.
commonly used sweetener in the U.S. diet is the disaccharide sucrose tie,
(table sugar), which contains 50% fructose and 50% glucose. However, in
North America and many other countries, non-diet soft drinks are sweetened
with high-fructose corn syrup (HFCS), which contains up to 55% of the
mono-saccharide fructose. Thanks to its abundance, sweetness, and low price,
HFCS has become the most common sweetener used in processed foods. It's not
that HFCS is biologically more ominous than sucrose; it's that its low cost
has made it available to everyone, especially low socioeconomic groups. HFCS
is found in processed foods ranging from soft drinks and candy bars to
crackers to hot dog buns to ketchup. Average daily fructose consumption has
increased by over 25% over the past 30 years. The growing dependence on
fructose in the Western diet may be fueling the obesity and type 2 diabetes
mellitus epidemics. Animal models demonstrate that high-fructose diets lead
to increased energy intake, decreased resting energy expenditure, excess fat
deposition, and insulin resistance, which suggest that fructose consumption
is playing a role in the epidemics of insulin resistance and obesity and
type 2 diabetes mellitus in humans. The metabolism of fructose differs
significantly from glucose. Fructose is absorbed in the intestine and enters
the liver without insulin regulation. There, fructose is converted to
fructose-1-phosphate and enters the metabolism without regulation. This
leads to an excess which cannot be metabolized, and it is then converted
into free fatty acids (which promote insulin resistance), very low-density
lipoproteins (VLDL, which promote atherogenesis and serve as a substrate for
obesity), and triglycerides. Fructose also does not suppress secretion of
the so-called "hunger hormone" ghrelin, levels of which correlate with
perceived hunger. In sum, fructose consumption has metabolic and hormonal
consequences that facilitate development of obesity and its complications.
The highest fructose loads are soda (1.7 gm/oz) and juice (1.8 gm/oz).
diet also tends to be poor in fiber, which may be one of the characteristics
that link it to obesity and insulin resistance. Cohort studies of young and
middle-aged adults demonstrate that fiber intake is inversely associated
with weight gain, fasting insulin levels, and risk of type 2 diabetes
mellitus. Generally, high fiber foods have low energy density. High-fiber
meals tend to be more satiating as they induce a greater sensation of
fullness than low-fiber meals. Fiber also slows gastric emptying.
Fiber-containing foods slow intestinal glucose absorption, which lessens the
after-meal insulin. Why is the Western diet fiber-poor? Because you can't
freeze and reheat fiber. Fast food must be shipped to franchises around the
world, thus the fiber must be removed first.
HOW DO YOU GET
THE INSULIN DOWN?
This is a difficult proposition,
given the current "toxic environment”. The UCSF Weight Assessment for Tee
and Child Health (WATCH) Program advocates
four simple rules for treating
by bringing the insulin down.
rid of every
sugared liquid in the house.
This means soda, juice, Kool-Aid, sports drinks, etc. Look at the bottle:
five calories per serving or less is OK; six or more, leave at
2) Eat your carbohydrates
with fiber. White food (bread, rice, pasta, potatoes) is fiberless food.
Brown food (brown rice, beans, lentils, peanuts, other legumes) is highfiber
food. Alternatively, look at the dietary fiber content: 3 g or more per
serving is adequate.
3) Wait 20 minutes for second portions. This takes advantage of
another hormone called peptide YY located in the distal intestine, which
acts as the satiety signal, preventing that second portion, and further
4) Get the TV out of the kid's room. And kids should buy their TV
time minute-for-minute with activity. Since when did TV watching become a
review, the mechanism of our "toxic environment's" effects on insulin and
weight gain in the genesis of obesity is elaborated. The composition of our
diet is highly insulinogenic. The insulin drives energy into fat, and
interferes with leptin signaling in the brain. This results in weight gain
and the sense of starvation reducing energy expenditure and physical
activity; and increased vagal activity, which promotes yet further insulin
release and energy storage. Thus, hyperinsulinemia turns the leptin negative
feedback system into a "vicious cycle" of obesity. Externally, this appears
as "gluttony and sloth," but it is biochemically driven.
How does this
work? A thin, insulin-sensitive, 13-year-old boy might consume a daily
allotment of 2,000 kcal, and burn 2,000 kcal daily (or 50 kcal/kg fat-free
mass) in order to remain weight-stable, with a stable leptin level. However,
if that same 13-year-old became hyperinsulinemic and/or insulin resistant,
perhaps as many as 250 kcal of the daily
allotment would be shunted to storage in adipose tissue, promoting a
persistent obligate weight gain. Due to the obligate energy storage, he now
only has 1,750 kcal per day to burn. The hyperinsulinemia also results in a
lower level of leptin signal transduction, conveying a CNS signal of energy
insufficiency. The remaining calories available are lower than his energy
expenditure; the CNS would sense starvation. He would reduce his physical
activity, resulting in decreased quality of life; and through increased
vagal tone, he would increase caloric intake and insulin secretion, but now
at a much higher level. Thus, the vicious cycle of gluttony, sloth, and
obesity is promulgated.
personal responsibility, when a kid's brain thinks it's starving? Is it
personal responsibility when the American Academy of Pediatrics still
recommends juice for toddlers? Is it personal responsibility when the Women,
Infant and Children program subsidizes fruit juice but not fruit? Is it
personal responsibility when the first ingredient in the barbecue sauce is
high-fructose corn syrup? Is it personal responsibility when high-fiber
fresh produce is unavailable in poor neighborhoods? Is it personal
responsibility when the local fast food restaurant is the only neighborhood
venue that is clean and air-conditioned? Is it personal responsibility when
in order to meet the criteria for No Child Left Behind, the school does away
with physical education class? Is it personal responsibility when children
are not allowed out of the house to play for fear of crime? We must get the
insulin down. Fixing the "toxic environment" by altering the food supply and
promoting physical activity for all children can't be done by government,
and won't be done by Big Food. This will require a grassroots, bottom-up
effort on the part of parents and community leaders.
Adapted from article written by Robert Lustig
MD in Pediatric Annals Dec 06
Simple solution for Obesity
Here are some simple guidelines for diet
and exercise I would like to share with you.
Eat only 6 things for breakfast, lunch and
- Grains and Vegetables (careful with corn
- Chicken (turkey ok)
Big breakfast, medium lunch, small dinner.
Nothing after 6 pm except water.
No fast food. Eat half of what restaurants
Do not eat anything that comes in a box.
No white foods
This provides carbs in their natural form.
This is how our great-great-great-great grandparents ate. You can give
alternatives: corn tortillas, brown rice, whole grain bread
The catch is that carb addiction is almost
an "all or none" phenomenon. If someone is dieting but decides to have a piece
of cake, this transitory hyperglycemia will release endorphins that will require
his/her body to "ask" for more.
Use a pedometer and get at least 10,000
steps daily. Limit the video games and TV. Get those teens one of those dance
revolution video game dance pads-- that will help them break a sweat....
Drink 8-10 glasses/day only water or diet drinks. No regular sodas or fruit
juices. Teenagers are consuming 1000+ calories (mostly carbs) in the form of
drinks (gatorade, kool aid, sodas, etc). When your fluid intake is only water
then you cut down 1000+ cal/day. That is 1 pound in 3 days only from drinks.
Sometimes we are thirsty instead of
hungry. When we drink water we cut some cravings. Water also helps constipation.
It flushes your toxins. Also you may have an acid heartburn stomach feeling
and think that you are hungry. Take an antacid with the water and that can help
On this diet kids can lose 10 lbs/ month
and so are their parents. Diets work if the whole family participate. It's not
about dieting for short term results, rather lifestyle change for sustained
improvement in health ... every day the rest of your life.
You can cut back eating for one week and
loose 1 lb and eat too much for just one day and put 1 lb back on. So people
think they starve all the time and not loose weight because they forget about
the one day they ate too much. You change your way of eating every day!
Loosing weight is like a marathon race.
You don’t run the first mile as fast as you can go or else you get tired too
soon and stop running. If you try to loose too much weight too fast, then you
will get exhausted and quit. Cut back the calories so you are loosing it 1-2 lb
a week. It will take a long time to get your weight down but since we are going
to change the way we eat for the rest of our lives…. Then it does not matter how
long it takes.
Studies showed that snacking was not as important contributor of over weight as
was fast food. So eating at home helps (family meals are very important), keep
low portion sizes, and no sweet drinks.
Calories in common drinks. snacks. and fast food:
20 oz Coke 250
(Grande) Caffe Latte
20 oz (Venti®)
16 oz Caffe Mocha
With whipped cream
20 oz Caffe Mocha
With whipped cream 490
20 oz original Orange Julius
32 oz original Orange Julius
20 oz BlackBerry Storm Smoothie
Candy bar; Snickers and Hershey's
1 oz bag of Lays Classic Potato Chips (20 chips) 150
1 oz bag of Doritos NACHO CHEESE'
1 oz bag
Corn Chips (32
McDonald's Quarter Pounder`"
McDonald's Big Mac°
Burger King Original Whopper"','
Original Recipe chicken drumstick
One Original Recipe chicken breast
McDonald's small fries 250
McDonald's medium fries
Burger King small fries
Burger King medium fries
Burger King large fries
King King-sized fries
slice of a Domino's 14" cheese pizza
1 slice of a Domino's 14" pepperoni pizza
slice of a Papa John's 14" cheese Pizzza
1 slice of a Papa John's 14" pepperoni pizza
slice of a Pizza Hut 14" cheese pizza
1 slice of a Pizza Hut 14" pepperoni pizza
Many restaurants will have a Web site that will list
nutritional information for their
items. Web sites can be found
the name of the franchise into a search engine such as
Other Web sites
calories in common foods include www.dietfacts.com, www.calorie-count.com,