ISIS Report 25/02/13
Fructose and Overeating - Fuelling the Obesity Epidemic
brain imaging study finds fructose, but not glucose,
causes distinct brain activity associated with a lack of fullness and satiety Dr. Eva Sirinathsinghji
fully referenced and illustrated version
of this article is posted on ISIS members website and is otherwise available
for download here
A new study finds that fructose consumption has distinct
effects on brain regions that regulate appetite, a possible mechanism for
‘ever-eating’ and the widespread rise in obesity and other related disorders.
study, led by Dr Robert Sherwin at Yale University in
the US, used magnetic resonance imaging (MRI) techniques to look at the
activity of brain regions associated with appetite and reward systems, to
assess how they respond to fructose versus glucose .
Dramatic increase in fructose consumption correlated with obesity
in fructose consumption have risen dramatically since the creation of high
fructose corn syrup (HFCS). HFCS has largely replaced table sugar as the most
common industrial sweetener, especially in the US where most processed foods
including soft drinks contain high levels of the
sugar substitute. Industrial-scale, cheap over-production of corn since the
Nixon era in the early 1970s laid the foundations for
the wide-spread use of HFCS, and this continues today with the US devoting
roughly a quarter of its agricultural land to corn crops, the majority of which
are now genetically modified (GM).
Rise in HFCS consumption over the last few decades appear to
correlate with the sharp increase in obesity and other diet-related disorders
including diabetes, suggesting fructose as a major contributory factor. The
HFCS used in beverages is usually 55 % fructose and 41 % glucose (HFCS55).
Since its introduction,
higher quantities of HFCS than sucrose is added despite it being sweeter
(sucrose is a disaccharide of both fructose and glucose). The excessive
consumption of fructose is therefore considered a major health risk.
Brains respond differently to fructose
the new study, 10 people consumed fructose or glucose drinks 15 minutes before
their brains were
analysed for cerebral blood flow, an indirect measure of brain activity. They then mapped out the regions of the brain with
significantly reduced blood flow; very different patterns emerged with the two
sugars (Figure 1).
Figure 1 Reduced
cerebral blood flow (marked in blue) after glucose (upper panel) and fructose
ingestion at different sections of the brain on fMRI
Glucose lowered cerebral blood flow in the hypothalamus, a region
that controls appetite and fuel sensing and regulates hunger, among other
metabolic processes including thirst, and circadian rhythm. Glucose also
reduced activity in other brain regions that are thought to act in synchrony to
read a person’s metabolic state and drive motivation and reward - the thalamus,
insula, anterior cingulate and striatum.
Fructose reduced activity in the posterior thalamus, the posterior
cingulate cortex, fusiform gyrus, visual cortex and the hippocampus, a region
most noted for its role in learning and memory and mediates emotional responses
to food. Hippocampal activity in rodents has previously been associated with
inhibition of feeding behaviour. Functional connectivity after fructose
consumption only increased between the hypothalamus and the thalamus.
Functional connectivity analysis was also carried out to identify
brain regions that are temporally and thus functionally related. Again the two
sugars gave very different patterns (Figure 2).
Figure 2 Functional
connectivity increase (bright yellow and red patches) after glucose (upper
panel) and fructose (lower panel) at different optical sections of the brain
Glucose increased functional connectivity between the hypothalamus
and the striatum and thalamus, other regions involved in feeding behaviour.
Fructose on the other hand, only increased functional connectivity between the
hypothalamus and the thalamus.
testing of the participants found that fructose led to reduced feelings of both
satiety and fullness.
Metabolic experiments found glucose but not fructose, to induce a
significant rise in blood insulin, a hormone that acts centrally to induce
satiety and dampen reward value of food. Lastly, they were able to detect
fructose in the brain of rodents following peripheral infusion of fructose,
showing its ability to penetrate the blood-brain barrier.
All together, these results indicate that the brain responds
differently to fructose, leaving individuals feeling less fulfilled and
therefore more susceptible to over-eating.
New study confirms previous findings
is not the first to establish a link between fructose and obesity/metabolic
disorders. A long-term feeding study in rats found that a 6-month high fructose
diet followed by a 2-week high fat diet led to weight gain
resulting from the development of leptin resistance during the high fructose
diet . Leptin is a hormone released by adipose tissue as a satiety signal
after eating. Fructose has also been shown to provoke feeding in rodents as
well as reduce circulating satiety-related molecules including insulin
and glucagon-like polypeptide 1 (GLP-1) .
fructose has been used by scientists as a tool for generating diabetes and/or
obesity animal models in research. Most recently, a
primate model of diabetes was induced by a high fructose diet. The rhesus
monkeys developed insulin resistance and many features of the metabolic
syndrome, including central obesity, dyslipidemia (abnormal blood lipid levels
e.g. cholesterol/fat) and inflammation within a short period of time;
moreover, a subset of monkeys developed type-2 diabetes . The authors went
on to suggest that due to the ‘rapidity with which the metabolic changes
occur’, that fructose consumption was a ‘practical and efficient’ system to
adopt for such research studies.
research studies have shown that fructose is metabolised in a different way
from glucose, with fructose having a higher propensity to be converted into
body fat, a process called lipogenesis. Prolonged fructose, but not glucose
consumption has been shown to induce de novo lipogenesis in the liver
. Similarly, it is thought to promote visceral over subcutaneous fat
deposition, a more common feature of metabolic disorders including diabetes
There are 5 comments on this article so far. Add your comment
|Stuart Krichauff Comment left 26th February 2013 09:09:41|
Was any differentiation between naturally occuring fructose and synthetic chemical corn fructose made.
Do primates on a natural fruit diet suffer the problems found in this article.
|Eva Sirinathsinghji Comment left 26th February 2013 19:07:21|
Stuart, thanks for the interesting question. I do not know of animals suffering from such diet-related problems. Many species including rhesus monkeys do however eat a variety of foods that contain fibre from fruit, nuts, seeds, roots, bark and leaves, which is thought to lower blood sugar levels. Many species also supplement their diets with other food types including insects and bird eggs. Soft drinks however, and many juices for that matter, do not contain the equivalent fibre content. Soft drinks also have very high levels of fructose. For example, an average can of soft drink contains 23g while a cup of tomatoes contains 2.5g so I think the amount and the context of how it is consumed is different between wild animals and manufactured food products which are far from representing a natural diet. There was no mention of any difference between natural vs synthetically made fructose but I would suspect that there would not be a difference.
|Rory Short Comment left 26th February 2013 14:02:20|
The same question as that of Stuart occurred to me, fruit eating bats do not have weight and diabetes issues as far as I know.
|Helen Comment left 28th February 2013 10:10:52|
There are several useful fructose content of foods database. Just google 'fructose counter' or 'sugar counter'.
|Gnarlodious Comment left 28th February 2013 21:09:08|
You forgot to explain that "corn syrup" is not actually made from corn. That was an appetizing deception cooked up by the ethanol industry to dispose of an otherwise toxic industrial by-product. "Corn syrup" is in fact the metabolic waste of bacterial digestion of corn. Any corn component of the syrup was already used up, and all you suckers are doing is slurping down aspergillus shit.