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The introduction of high fructose corn syrup (HFCS) in the seventies coincided with a marked rise in obesity in the U.S., leading to speculations that there might be a causal connection between HFCS consumption and weight gain. This seemed all the more plausible since HFCS consumption grew much faster than any other food intake.
On the other hand, obesity rates also increased in Europe and other parts of the world where sucrose (table sugar) remained the major caloric sweetener. This seemed to argue against a connection between HFCS and weight gain, particularly since the fructose/glucose ratios of high fructose corn syrup and sucrose are quite similar.
What sucrose and high fructose corn syrup have in common, and what distinguishes them from dietary carbohydrates such as starch, is their fructose content. Fructose contributes the same amount of energy as glucose, but it doesn′t trigger the same satiety signals. The sharp rise in the consumption of soft drinks and processed foods sweetened with HFCS and sucrose led to a dramatic increase in fructose intake, a source of energy that goes essentially unnoticed.
What is high fructose corn syrup?
High fructose corn syrup is made from corn starch, a glucose polymer. First, enzymatic starch breakdown yields corn syrup which is essentially free glucose. The glucose is then further enzymatically converted to fructose. After various purification steps, a mixture of 90% fructose and 10% glucose (HFCS-90) is obtained. HFCS-90 is mixed with appropriate amounts of corn syrup to make either HFCS-55 or HFCS-42, mixtures with 55% and 42% fructose, respectively. HFCS-55 is mainly used for soft drinks, whereas HFCS-42 is primarily used to sweeten baked goods.
Not only are sucrose and high fructose corn syrup similar in their fructose/glucose ratios, but soft drinks are acidic enough to hydrolyze sucrose. An analysis of sucrose-sweetened soft drinks showed that ten days after manufacture only 50% of the sucrose was still intact. After three months 90% of the sucrose was hydrolyzed, i.e. even sucrose-sweetened soft drinks contain mostly free fructose and glucose.
HFCS has largely replaced sucrose in commercial foods in North America. It is cheaper than sucrose, partly because of import tariffs on sucrose and agricultural subsidies to corn producers.
HFCS versus sucrose in drinks - is there a difference?
37 men and women in their twenties and in the healthy weight range were recruited to compare the effects of soft drinks sweetened with sucrose and HFCS on subsequent food intake. At mid-morning the participants were given one of six preloads: 215 kcal from sodas sweetened with sucrose, HFCS-42, or HFCS-55, 215 kcal from 1% milk, 4 kcal from aspartame-sweetened diet soda, or no drink at all. Later all subjects were given the same lunch and they were free to eat as much as they wanted. Leftover food was weighed, giving the investigators an accurate measure of energy intake. Averaged over six lunches, the following total calorie intakes (in kcal) from preload plus lunch were found: HFCS-42 1193, HFCS-55 1182, sucrose 1170, 1% milk 1129, aspartame 1011, and no drink 1008.
Clearly, there was no signficant difference between the sodas sweetened with sucrose and those with HFCS. In addition, the subjects drinking caloric preloads clearly took in more total calories than those drinking the low-cal soda or nothing at all. In other words, those who had caloric drinks before lunch did not reduce their food intake sufficiently to compensate for the preload.
Sugars in solid versus liquid form - does it matter?
To answer this question, 15 men and women were recruited for a short cross-over trial designed to compare the effects of equicaloric liquid and solid carbohydrate sweeteners on food intake. All participants were in their twenties and in the healthy weight range.
The trial consisted of two four-week interventions, separated by a four-week washout period and cross-over. Once a week during the two trial phases the participants presented themselves to the investigators to be weighed and supplied with weekly rations of their daily 450 kcal sweeteners. The solid load consisted of sucrose-sweetened jelly beans, and the liquid load of 
HFCS-sweetened soda.
The participants were free to decide when to take their daily loads, and when and what to eat. Calorie intake was estimated from self-assessments of food consumption.
Analysis of the food questionnaires indicated that during their solid phase the subjects fully compensated for the energy content of their preload; the total calorie intake from food plus test sweetener was equal to the pre-trial food energy intake. This was not the case, however, during their liquid trial phase, where food intake remained unchanged, i.e. the sweetened drink added to the total calories.
While conclusions based on self-reporting of food eaten are always questionable, these were within-subject comparisons, i.e. the same bias was likely present in their estimate of food intake after liquid and after solid preloading. Furthermore, the estimated energy intakes were consistent with measured changes in body weight. The participants experienced significant weight gains during the liquid trial phase, but not during the solid trial phase, consistent with an excess energy intake in the liquid phase.
It appears therefore that caloric sweeteners contribute to weight gain if consumed in drinks, but not in solid food.
Fructose and glucose affect appetite and food intake differently.
Two hormones, insulin and leptin, act as satiety signals in the brain and thus are critical to energy homeostasis. Both insulin and leptin circulate in the blood at levels proportional to body fat content, and enter the central nervous system in proportion to their plasma levels. Low hormone levels increase appetite, and high levels act to reduce energy intake.
Insulin levels rise in response to blood glucose. Insulin-mediated entry of glucose into adipocytes (fat cells) in turn causes the release of leptin. In other words, both insulin and leptin levels react to glucose concentrations. Fructose, on the other hand, does not trigger insulin release. This in turn means that fructose doesn′t affect leptin levels either. Since it increases neither insulin nor leptin levels, fructose consumption does not generate the same satiety signals as glucose. The result is overeating and weight gain.
To summarize, the rise in obesity rates with increasing HFCS consumption was no coincidence. The increased popularity of soft drinks and HFCS-sweetened convenience foods led to a rapid increase in fructose consumption. It was this excessive fructose intake that fuelled the rapid weight gain, since fructose does not generate the same satiety signals as glucose. It is likely that sweetened drinks are worse than sweet solid foods, and that sucrose has the same effect as high fructose corn syrup.
Most studies of the effects of calorically sweetened liquids on appetite and weight gain looked at soft drinks. However, fruit juices and drinks also contain added sweeteners, typically HFCS, i.e. they pose the same obesity risk. Switching to noncalorically sweetened soft drinks isn′t the answer either, since artificial sweeteners like aspartame come with problems of their own.
Of course fruit also contains fructose ("fruit sugar"), but this obviously doesn′t mean that one should stop eating fruit. It doesn′t contain nearly as much fructose as sweetened drinks and it is a valuable source of phytonutrients and fiber, whereas soft drinks provide little more than empty calories.
Clearly, one of the best things we can do for our health is to stop drinking soft drinks.
Ref: naturalnews.com
Also Read: Soft Drinks - Hard Facts!
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