Guest Blogger: I
am very happy to introduce Ruby Schuler as a guest blogger. Ruby was
one of my fabulous fourth graders. She was a superstar even at the age
of nine.
High-fructose corn syrup (HFCS) can be
found in various products such as cookies, sodas, crackers, and cereals. This
can make it hard to avoid when consuming processed foods and drinks.1 With all of the negative media attention HFCS gets, it is easy to think that it
is not the healthiest of substances, yet it is hard to determine why HFCS is
not healthy. Have you ever wondered why HFCS is in our food products instead of
sugar? Is HFCS worse, health-wise, than table sugar? Is HFCS responsible for
our country’s obesity epidemic? Take a look at the facts.
HFCS is now commonly used in foods in
lieu of table sugar (sucrose) because it is cheaper and more stable.2,3 More than half of the sugar in the United States is derived from the
sugar beet, which is grown in the cooler climates of the Midwest states.4 HFCS is made from American corn which is overly abundant and extremely cheap
due to government subsidies.2 HFCS is a much more stable compound than table sugar for processed foods and
beverages because it can withstand the acidic conditions these products go
through when being shipped and subsequently left to sit on the shelf in a
warehouse or grocery store.3 The stability of HFCS is due to its slightly different chemical composition in
comparison to sucrose. Sucrose is a disaccharide, meaning that it is composed
of two different single sugars, which are connected. These two single sugars
are known as glucose and fructose. HFCS is made up of glucose and fructose as
well; however, in HFCS these two molecules are not connected.1,3 The way in which HFCS is made is what makes the difference in composition. The
process of making HFCS was perfected in the late 1960’s in Japan and involves a
multiple-use enzyme that catalyzes the conversion of about half of the glucose
in corn into fructose. HFCS is made up of an almost 50:50 ratio of glucose to
fructose, the same ratio as sucrose.1,2,5
The difference in the chemical structures
between HFCS and sucrose has led some researchers to believe that HFCS is
metabolized differently than sucrose by the body and therefore could be a cause
for concern in its relationship to obesity in the United States.1,3,6 HFCS is made up of free––not connected, as in sucrose––glucose and fructose
molecules.1,3 Glucose is important in signaling the regulating hormone insulin, which
triggers either the release or inhibition of two other hormones that are
important in appetite and satiety. These two hormones are ghrelin, which is
responsible for telling your body when it is hungry and inhibited by insulin,
and leptin, which is responsible for signaling to your body that it is
full. It is released by the presence of insulin, thus causing you to want
to stop eating. Fructose, on the other hand, does not signal insulin to be
secreted, so leptin will not be triggered; your body will not tell you when it
is full.1,6 The
lack of insulin secretion also leads to the buildup of fructose in the liver,
because the fructose won’t be able to be taken up by other tissues in your body
without insulin present in your bloodstream. Your body wants to use this
buildup of sugar for energy before it uses the fat in your body for energy,
which can lead to weight gain due to this hierarchy of oxidation. Several
recent studies have shown that fructose specifically increases visceral fat, or
the fat that surrounds your organs in the abdominal area.7 This may be due to the structure of fructose which allows for it to bypass an
important regulating step in the liver. By bypassing this step, the liver then
uses the fructose in other forms to create more fat.9 This is cause for concern due to the negative effects this belly fat can have
on the body, mainly increasing risks for type 2 diabetes and heart disease.7
Observational data is what sparked the
original hypothesis that HFCS was related to the rising obesity epidemic in the
United States. The frequent use of HFCS in products in the United States really
took off in the late 1960’s; around the time its production method was being
perfected. Obesity began to rise at approximately the same time as the increase
in use of HFCS, causing some researchers to think that HFCS could be the cause
of the obesity epidemic.1 Some experiments have investigated the hypothesis that HFCS could be
responsible for the increase in obesity; however, their results have shown that
the hormones insulin, ghrelin, and leptin are not affected any differently then
they are by sucrose.6,8
Studies have been carried out showing that the consumption of sugary
beverages, both increase visceral fat, whether sweetened with HFCS or sucrose.7
More research is needed in order to
completely understand the effects HFCS has on the body. In recalling that HFCS
and sucrose are both composed of the same molecules, glucose and fructose, it is
important to remember that the unbound form of fructose found in HFCS could
potentially be where the most devastating effects to the body occur due to the
bypassed regulation of fructose in the liver. By consuming most sugar through
whole foods, such as fruits and vegetables, along with restricting the amount of
processed foods in the diet, the harmful affects of sugar can be reduced. Those
who wish to avoid weight gain should be more concerned with the amount of added
sugars they are consuming (like those in processed foods and drinks) instead of
the specific type, namely the amount of fructose, which has been shown to
increase harmful belly fat.10
Ruby Schuler is a senior year at UC
Berkeley, majoring in Nutritional Science, Dietetics. She is interested in
helping others learn about the immense power food has on our bodies, either
beneficial or detrimental. Ruby knows that there is a lot of information
about nutrition floating around in the media. She thinks it's
important to remember that decisions about your health should be made from
reliable sources. This information can be hard to come by, but she hopes
to be one of the many people who can supply you with evidence to help you make
better choices that can result in living a healthier and happier life!
1. Bray, G. A.,
Nielsen, S. J., & Popkin, B. M. (January 01, 2004). Consumption of
high-fructose corn syrup in beverages may play a role in the epidemic of
obesity. The American Journal of Clinical Nutrition, 79, 4, 537-43.
2. Casey, J. P.
(January 01, 1977). High Fructose Corn Syrup. A Case History of Innovation.
Starch - Stärke, 29, 6, 196-204.
3. White, J. S.
(January 01, 2008). Straight talk about high-fructose corn syrup: what it is
and what it ain't. The American Journal of Clinical Nutrition, 88, 6.
4. Ali, Mir B.
(October 01, 2004). Characteristics and Production Costs of U.S. Sugarbeet
Farms. United States Department of Agriculture: Economic Research Service,
974-8
5. Bemiller, J.
N. (September 23, 2009). One hundred years of commercial food carbohydrates in
the United States. Journal of Agricultural and Food Chemistry, 57, 18,
8125-8129.
6. Melanson, K.
J., Zukley, L., Lowndes, J., Nguyen, V., Angelopoulos, T. J., & Rippe, J.
M. (February 01, 2007). Effects of high-fructose corn syrup and sucrose
consumption on circulating glucose, insulin, leptin, and ghrelin and on
appetite in normal-weight women. Nutrition, 23, 2,
103-112.
7. Liebman,
Bonnie (April 01, 2012). Sugar Belly: How Much Sugar is Too Much Sugar? Nutrition
Action, 3-7.
8. Stanhope, K.
L., Swarbrick, M. M., Havel, P. J., Bair, B. R., Griffen, S. C., & Keim, N.
L. (May 01, 2008). Twenty-four-hour endocrine and metabolic profiles following
consumption of high-fructose corn syrup-, sucrose-, fructose-, and
glucose-sweetened beverages with meals. American Journal of Clinical Nutrition,
87, 5, 1194-1203.
9. Elliott,
S.S., Keim, N.L., Stern, J. S., Teff, K., Havel, P.J. Fructose, weight
gain, and the insulin resistance syndrome. Am J Clin Nutr November
2002 vol. 76 no. 5 911-922.
10. White,
J.S. Straight talk about high-fructose corn syrup: what it is and what it
ain't. Am J Clin Nutr December 2008 vol. 88 no. 6 1716S-1721S.
The difference in the chemical structures
between HFCS and sucrose has led some researchers to believe that HFCS is
metabolized differently than sucrose by the body and therefore could be a cause
for concern in its relationship to obesity in the United States.1,3,6 HFCS is made up of free––not connected, as in sucrose––glucose and fructose
molecules.1,3 Glucose is important in signaling the regulating hormone insulin, which
triggers either the release or inhibition of two other hormones that are
important in appetite and satiety. These two hormones are ghrelin, which is
responsible for telling your body when it is hungry and inhibited by insulin,
and leptin, which is responsible for signaling to your body that it is
full. It is released by the presence of insulin, thus causing you to want
to stop eating. Fructose, on the other hand, does not signal insulin to be
secreted, so leptin will not be triggered; your body will not tell you when it
is full.1,6 The
lack of insulin secretion also leads to the buildup of fructose in the liver,
because the fructose won’t be able to be taken up by other tissues in your body
without insulin present in your bloodstream. Your body wants to use this
buildup of sugar for energy before it uses the fat in your body for energy,
which can lead to weight gain due to this hierarchy of oxidation. Several
recent studies have shown that fructose specifically increases visceral fat, or
the fat that surrounds your organs in the abdominal area.7 This may be due to the structure of fructose which allows for it to bypass an
important regulating step in the liver. By bypassing this step, the liver then
uses the fructose in other forms to create more fat.9 This is cause for concern due to the negative effects this belly fat can have
on the body, mainly increasing risks for type 2 diabetes and heart disease.7 
If you live in northern latitudes, above
the 37th
parallel (which in the United States, extends from San Francisco, CA over
to Newport News, Virginia), the angle of the sun is so low that hardly any
Vitamin D can be produced in the skin between November and February, with other experts saying that October to April, is probably more accurate.
For adults who need to take a Vitamin D3 supplement, Holick recommends 2,000 IU per day with a safe upper limit of
10,000 IU/day depending on individual need. To consume the recommended 2,000 IU of Vitamin D in your
diet, you would need to drink 20 glasses of fortified milk, eat 6 cans of
sardines, 100 egg yokes, 7 oz of wild salmon or 20 bowls of fortified cereal
each day. This is clearly a nutrient we were meant to get from the sunshine.
Vitamin D can influence if a cell will
become cancerous or not. If it does
become cancerous, not only can it prevent the malignant cells from reproducing,
but it can also help kill the cell or cut off the blood supply to the
tumor. Holick believes that “anytime you become vitamin D-deficient,
you put yourself at increased risk of potentially developing a malignancy
because you’ve lost the policing ability of vitamin D to help keep cell growth
in check.”
Research has also shown casein to act as
a histamine releaser. Histamine is a chemical in the body associated with
allergic reactions and can contribute to an inflammatory response.
