"Glycemic load" of diet has no effect on weight loss
"Glycemic load" of diet has no effect on weight loss
By Amy Norton
Thu Apr 19, 11:44 AM ET
NEW YORK (Reuters Health) - When it comes to losing weight, the number of calories you eat, rather than the type of carbohydrates, may be what matters most, according to a new study.
The findings, published in the American Journal of Clinical Nutrition, suggest that diets low in "glycemic load" are no better at taking the pounds off than more traditional -- and more carbohydrate-friendly -- approaches to calorie-cutting.
The concept of glycemic load is based on the fact that different carbohydrates have different effects on blood sugar. White bread and potatoes, for example, have a high glycemic index, which means they tend to cause a rapid surge in blood sugar. Other carbs, such as high-fiber cereals or beans, create a more gradual change and are considered to have a low glycemic index.
The measurement of glycemic load takes things a step further by considering not only an individual food's glycemic index, but its total number of carbohydrates. A sweet juicy piece of fruit might have a high glycemic index, but is low in calories and grams of carbohydrate. Therefore, it can fit into a diet low in glycemic load.
However, the effort of figuring out what's an allowable carb might not be worth it, if the new study is any indication.
Principal investigator Dr. Susan B. Roberts, of Tufts University, Boston, and colleagues found that a reduced-calorie diet, whether glycemic load was high or low, was effective in helping 34 overweight adults shed pounds over one year.
Study participants who followed a low-glycemic-load diet ended up losing roughly 8 percent of their initial weight, as did those who followed a high-glycemic-load diet.
"The bottom line is that in this study we don't see one single way to eat that is better for weight loss on average," Roberts told Reuters Health. Of course, that doesn't mean "anything goes" as long as you're cutting calories."
A super-sized serving of French fries won't do any dieter any good, she noted.
Both diets her team used in the study were carefully controlled. For the first 6 months, participants were provided with all the food they needed, and both diets were designed to cut their calories by 30 percent while providing the recommended amount of fiber, limiting fat and encouraging healthy foods like fruits and vegetables.
The comparable outcomes suggest that, among healthy diets, no single one stands out as better, according to Roberts. So the focus should be on calories, rather than specific foods to avoid or include.
"Focusing on calories is something we need more of, especially when portion sizes are so absurd," Roberts said, referring to the portions served at so many U.S. restaurants.
This doesn't mean, however, that there's no place for diets that focus on glycemic load, according to the researcher. Some studies, for example, have found that low-glycemic index foods might help control blood sugar in people with type 2 diabetes.
And in their own research, Roberts said she and her colleagues have found that low-glycemic index diets do seem more effective for overweight people who naturally secrete high levels of the hormone insulin, which regulates blood sugar.
SOURCE: American Journal of Clinical Nutrition, April 2007.
This is about the same study with a little additional info.
Hmmm. Glycemic Load. No Effect on Weight Loss
by Charles Stuart Platkin
A new study examined calorie restriction and glycemic load and found no difference in those that used the GL and those that didn't in long term weight loss. Read on...
Boston — The first phase of a caloric restriction study in human subjects at the Jean Mayer US Department of Agriculture Human Nutrition Research Center on Aging (USDA HNRCA) at Tufts University found evidence suggesting that calorie-restricted diets differing substantially in glycemic load can result in comparable long-term weight loss. The study, part of the multi-center Comprehensive Assessment of Long-term Effects of Restricting Intake of Energy (CALERIE) trial, funded by the National Institute on Aging, accounted for dietary factors that affect hunger and satiety, used laboratory techniques to measure adherence, and was the first of its kind to provide a complete set of meals and snacks to its participants. Recruitment is currently underway for participation in the second phase of the CALERIE study at Tufts, which will examine the relationship between calorie-restricted diets, aging, and age-related disease.
"Participants in our pilot study achieved and maintained comparable weight loss after one year, regardless of whether they were on a low-glycemic-load or a high-glycemic-load diet," says corresponding author Susan Roberts, PhD, director of the USDA HNRCA's Energy Metabolism Laboratory. "The goal was for both groups to restrict calories by 30 percent and, after one year, both groups had lost an average of 8 percent of their original body weight. We found that the two groups did not differ significantly in their average body fat loss, energy intake, metabolic rate, or reports of hunger and satiety."
The two study diets were carefully matched for factors known to influence food intake during weight-loss efforts, such as palatability, dietary variety, and fiber. "Because there was careful attention to factors that influence hunger and satiety, participants were generally satisfied on a calorie-restricted diet," says Roberts, who is also a professor at the Friedman School of Nutrition Science and Policy at Tufts.
Thirty-four overweight but otherwise healthy men and women were assigned randomly to a low-glycemic-load (LG) or high-glycemic-load (HG) diet. At six months, the LG group had lost an average of 10.4 percent body weight, while the HG group had lost an average of 9 percent body weight. By 12 months, participants in both the LG and HG groups had lost an average of 8 percent of their starting body weight.
"Unlike several other long-term studies, which have reported greater weight loss with low GL diets at six months but no differences by 12 months, our data show no significant short-term or long-term differences," notes Sai Das, PhD, scientist at the USDA HNRCA and first author of the study. "However, we did detect a greater tendency for weight and body-fat regain among LG participants. This finding suggests that reduced calorie intake may be harder to sustain on LG diets over time."
The LG diet contained 40 percent carbohydrate, 30 percent fat, and 30 percent protein; while the HG diet contained 60 percent carbohydrate, 20 percent fat, and 20 percent protein. A food's glycemic load is a relative measure of how much carbohydrate is in the food and how quickly that food is converted in the body to blood sugar. Examples of foods provided as part of the LG diet include bean and barley stew, low-fat cottage cheese, and pumpernickel bread. The HG diet included foods like bagels, candied sweet potatoes and shepherd's pie with mashed potatoes.
Both diets were designed to restrict calories by 30 percent, relative to a person's baseline energy requirements, while providing the recommended amounts of vitamins, minerals, and essential fatty acids. All participants attended weekly behavioral support groups and met individually with a dietitian.
To measure objectively actual dietary intakes, the researchers used a laboratory technique involving doubly labeled water. They determined that both groups ate more calories than study foods provided; at six months the HG group averaged a 16 percent calorie-restricted diet and the LG group averaged a 17 percent calorie-restricted diet. Although participants did consume additional calories, the degree of non-adherence was not significantly different between the LG and HG groups when measured at various points throughout the study.
"An important difference between our study and other weight-loss trials is that we did not rely on self-reported intakes," says Das, who is also an assistant professor at the Friedman School. "Underreporting of caloric intake can vary between 5 and 50 percent. By providing the study food for the first six months, we did not have to worry as much about lifestyle factors like shopping and cooking habits interfering with dietary change."
Roberts previously conducted a pilot study showing that a diet's overall glycemic load may be an important determinant of weight loss for people with high levels of insulin secretion, such as people with diabetes. "We have observed that for some groups, glycemic load may impact weight loss. However, in terms of calorie-restricted diets, we see little difference among diets of varying glycemic load when we account for factors that affect dietary adherence."
This info seems a little misleading to me. Notice both articles refrence "Weight Loss" not FAT LOSS, that is a big problem right off the bat. I agree that total cals will be a larger factor then types of carbs that are consumed, but when your talking about fat loss, it is very important to keep blood glucose levels stable. This is very hard to do with the inclusion of only high GI carbs in your diet.
I dont think either of you will disagree that low GI carbs have many more health benifits then do high GI carbs. And it is very easy to misconstrue the info that is in this article. I personally wont be trading in my oatmeal for a snickers anytime soon, and I would hope those who read this understand that this isnt exactly evidence of anything.
Hell, I could go on an all sugar diet and lose 40lbs in the next month, doesnt mean its healthy, or that I will have any muscle mass left at the end of it.
It's just info. I'm certainly not saying people should eat a bunch of high GI or GL carbs.
It is, however, info aimed at the general public. And no matter how a bodybuilder may look at it, the average person doing some type of fad diet is experiencing WEIGHT loss, not just FAT loss. Sorry but it's true. Furthermore if you look at ANY fad diet, high protein, whatever, they all have in common a calorie deficit. Some of them RIDICULOUSLY low. Low enough to guarantee both muscle and fat loss regardless of whatever gimmick the diet is based around. But is also depends how much fat we're talking about. Because if there is enough fat involved then a simple energy deficit is going to be mostly fat loss.
The main cause of so-called metabolic syndrome is being overweight/obese and physically inactive. A lot of people will say it the other way around because they want to sell you something. They'll say metabolic syndrome causes your overweigtness. That may be true for some individuals with genetic factors but their principal reason for saying it is to make you think you're inability to lose weight is out of your control because of your "metabolic" problems. So enter "product X."
I do think that people are putting a little to much nit picking thought into insulin control. They are taking information about a hoast of metabolic disorders, some of them unrelated, and then applying them to a pysically fit person who is healthy. You take a person who is obese and desparately needs to lose weight the fact is that losing all that excess fat is going to do a WHOLE lot more toward curing their insulin resistance than whether they ate high or low GL carbs during the diet. And if they are able to keep the fat off in the long run then all the better. This is the main therapy, in fact, weight loss and exercise.
It would be much better for them to retain muscle but I still don't see how the GL of the carbs will keep them from retaining muscle during a slow steady weight loss if they are not on too low an energy deficit and are weight training. I'm not saying they should be eating a bunch of high GL carbs either. And just keeping the weight loss slow and steady in itself assures better lean mass retention.
What applies to some guy cutting because he wants to see his six-pack and is essentially on a crash diet doesn't really apply to someone with a real weight problem.
For me I agree it doesn't prove anything. But neither does all the other "theory" regarding fat loss that so many take for the gospel.
BTW, for GLYCEMIC LOAD, high is anything over 20. GL of 20 or more is high, a GL of 11 to 19 inclusive is medium, and a GL of 10 or less is low. And to determine it you take the glycemic index of the food, divide by 100 and multiply it by carbohydrate amount.
Again, let me be clear, I just thought it was an interesting result. I'm not trying to say people should be consuming high GL diets.
For the average person glycemic load really dosen't make much of a difference. Calories in vs calories out will do it. Not quite the same for the serious bodybuilder.
Low-Glycemic Load Diet vs. Low Fat Diet w/High Insulin
Low–Glycemic-Load Diet Better Than Low-Fat Diet for Weight Loss in Those With High Insulin Secretions CME
News Author: Shelley Wood
CME Author: Désirée Lie, MD, MSEd
Release Date: May 16, 2007;
from Heartwire — a professional news service of WebMD
May 16, 2007 — Individual differences in insulin secretion may explain why some individuals respond well to either a low-fat diet or low–glycemic-load diet, whereas others do not, a randomized study suggests. The findings imply that a simple, baseline oral glucose tolerance test to assess serum insulin concentration may help clinicians and dieticians choose weight-loss strategies for obese subjects.
Cara B. Ebbeling, PhD, from Children's Hospital Boston, in Massachusetts, and colleagues, report the results of their study in the May 16 issue of JAMA.
"We often ask, why do people succeed with a conventional low-fat diet while others who are following the exact same diet can't keep weight off?" Dr. Ebbeling told heartwire. "Usually we answer this question with something like: 'the ones who succeed are more motivated, or have more willpower, or they're more able to stick with a diet while others are not as motivated.' But this really is not a complete answer to the question. So we sought to determine if biology had something to do with it."
Ebbeling and colleagues randomized 73 obese young adults (aged 18 - 35 years) to a 6-month dietary intervention: either a low–glycemic-load diet (40% carbohydrate, 35% fat, and rich in low–glycemic index foods), or a low-fat diet (55% carbohydrate and 20% fat). At baseline, all subjects were given an oral glucose tolerance test to check for insulin concentration after 75 g of dextrose. Subjects adhered "intensively" to diets for 6 months, then were followed up for an additional 12 months.
For the group as a whole, changes in body weight and body fat percentage at 18 months did not differ between the 2 diet groups; however, when stratified according to baseline glucose tolerance test, subjects with above-median insulin concentration (> 57.5 µlU/mL) lost significantly more weight on the low–glycemic-load diet than they did on the low-fat diet by 18 months. In contrast, subjects with insulin concentrations below median levels (≤ 57.5 µlU/mL) during the baseline glucose tolerance test had similar outcomes, regardless of to which diet they had been randomized.
Table 1. Changes by Diet After 18 Months, Above Median Insulin Concentration Subjects
Outcome Low–Glycemic-Load Diet Low-Fat Diet P
Weight change, kg -5.8 -1.2 .004
Body fat, % -2.6 -0.9 .03
Source: JAMA. 2007;297:2092-2102.
Differences between the diets were seen in effects of the different diets on lipid parameters, regardless of baseline glucose tolerance tests. The low–glycemic-load diet produced significant improvements in high-density lipoprotein (HDL) cholesterol and triglyceride profiles, whereas the low-fat diet produced significantly greater reductions in low-density lipoprotein (LDL) cholesterol levels.
"Regardless of insulin secretion at baseline, the LGL [low–glycemic-load] diet has beneficial effects on HDL cholesterol and triglycerides that were not seen on the LF [low-fat] diet, while LDL cholesterol decreased in the participants in the LF diet, but not the LGL diet," Dr. Ebbeling said. "This is just is speculation on our part, but an LGL diet that also substitutes unsaturated fats for fats may be even more beneficial for everyone, since the beneficial effects on insulin, cholesterol, and triglycerides with the LGL diet were seen regardless of insulin secretion."
Table 2. Lipid Changes by Diet, Entire Cohort*
Parameter Low–Glycemic- Load Diet Low-Fat Diet P
LDL, mg/dL -5.8 -16.3 .03
HDL, mg/dL 1.6 -4.4 .002
Triglycerides, %† -21.2 -4.0 .02
*LDL indicates low-density lipoprotein cholesterol; HDL, high-density lipoprotein cholesterol.
†mg/dL measurements log-transformed to percentages to reduce skew.
Source: JAMA. 2007;297:2092-2102.
Spikes in insulin concentration after a meal are believed to promote feelings of hunger and can lead to overeating, Dr. Ebbeling told heartwire. "People who are 'high insulin secreters' may be particularly susceptible to weight gain with conventional low fat diets that are higher in carbohydrates." By contrast, low insulin secreters seem to do the same on either the low-fat diet or the low–glycemic-load diet, she continued. "It seems that people who are high insulin secreters may be particularly susceptible to weight gain and may be more challenged to lose weight with a conventional low fat diet."
Of note, in survey questions assessing levels of satisfaction with the diets or with degree of weight loss, or probing ease or palatability of the diets, study subjects responded similarly to both questions.
"From a clinical perspective, our findings provide rationale for individualizing weight loss diets or diet prescription based on an oral glucose tolerance test," Dr. Ebbeling told heartwire.
According to the authors of the current study, 3 popular diets (low fat, low glycemic load, and low carbohydrate) have received attention recently for addressing obesity, but results of trials have been inconsistent because of different physiologic responses of participants. For example, individuals with different insulin secretion in response to a glucose load may respond differently to a low–glycemic-index diet. According to the authors, benefits of low–glycemic-load or low-carbohydrate diets have been shown in relation to components of the metabolic syndrome.
This is a randomized trial conducted in obese young adults with similar education, treatment intensity, and physical activity to examine whether a low–glycemic-load diet vs a low-fat diet is associated with differential weight and lipid outcomes.
*Included were adults aged 18 to 35 years with a body mass index of 30 kg/m2 and above and clearance from their clinicians.
*Excluded were current smokers and those with weight exceeding 140 kg, recent weight-loss diet, or diabetes mellitus.
*Prior to randomization, all participants underwent a 75-g glucose tolerance test, and glucose levels, insulin levels at 30 minutes, and lipids were measured.
*The dietary intervention had a 6-month intensive period followed by 12 months of follow-up.
*Measurements were repeated at 6, 12, and 18 months and body weight was tracked.
*Physical activity level and satisfaction with the program were assessed.
*The low–glycemic-load diet (n = 36) comprised nonstarchy vegetables, legumes, healthful nuts, and temperate fruits, limiting intake of high glycemic index foods such as refined grains, starchy vegetables, and fruit juices. 40% of energy was from carbohydrates, 35% from fat, and 25% from protein.
*The low-fat diet (n = 37) comprised 55% carbohydrate, 20% fat, and 25% proteins with an emphasis on low-fat grains, vegetables, fruits, and legumes.
*Participants in both groups received food-choice lists, had serving sizes defined, and received similar nutritional counseling.
*Education was offered in workshops with a total of 23 workshops, 1 private counseling session, and 5 motivational telephone calls for each participant.
*Dietary intake was assessed by the Nutrition Data System for Research Software.
*Dietary variables examined included carbohydrates, fat, protein, and fiber intake.
*Dietary glycemic index and load were quantified by a prespecified method using existing glycemic index values for foods.
*Glycemic load was calculated as the product of the daily glycemic index and total carbohydrate intake and adjusted for energy intake.
*Primary outcomes were weight loss, body fat percentage using dual energy x-ray absorptiometry, and cardiovascular disease risk factors such as lipid profile.
80% were women, 55% were white, mean age was 28 years, mean weight was 103 kg, mean body fat percentage was 41%, and mean blood pressure was 105 mm Hg systolic and 63 mm Hg diastolic.
*Fasting insulin level and trunk fat were higher in those with high insulin levels at 30 minutes after the 75-g glucose load.
*Treatment intensity was similar in the 2 groups, and the 2 groups differed in diet composition as expected.
*Weight loss did not differ for the full cohort of 73 patients.
*Insulin level 30 minutes after the glucose load was a significant modifier of the weight loss effect.
*For those with insulin concentration above the median of 57.5 µIU/mL, the low–glycemic-load diet produced a greater weight loss (-5.8 vs -1.2 kg; P = .004) and body fat percentage (-2.6% vs -0.9%; P = .03) vs the low-fat diet at 18 months.
*The net mean difference was -2.2 kg for each 2-fold increase in insulin concentration at 30 minutes.
*Those with low insulin levels after the 75-g glucose load showed no difference in weight loss between the low–glycemic-load and low-fat diets.
*Body fat percentage decreased more in those with high insulin concentration at 30 minutes for the low–glycemic-load vs the low-fat group.
*The insulin concentration at 30 minutes after a glucose load was not a modifier of lipid effects, blood pressure, fasting glucose levels, or fasting insulin levels.
*Plasma HDL cholesterol and triglyceride levels improved more with the low–glycemic-load diet, whereas LDL cholesterol levels improved more with the low-fat diet.
Bumping this for fun. Again, none of this is to be construed as having anything to do with "cutting". Although some of it may point out the fact that different people have different needs.
On a related note...the fructose discussion.
The Double Danger of
High Fructose Corn Syrup
By Bill Sanda, BS, MBA
For many years, Dr. Meira Fields and her coworkers at the US Department of Agriculture investigated the harmful effects of dietary sugar on rats. They discovered that when male rats are fed a diet deficient in copper, with sucrose as the carbohydrate, they develop severe pathologies of vital organs. Liver, heart and testes exhibit extreme swelling, while the pancreas atrophies, invariably leading to death of the rats before maturity.
Sucrose is a disaccharide composed of 50 percent glucose and 50 percent fructose. Dr. Fields repeated her experiments to determine whether it was the glucose or fructose moiety that caused the harmful effects. Starch breaks down into glucose when digested. On a copper-deficient diet, the male rats showed some signs of copper deficiency, but not the gross abnormalities of vital organs that occur in rats on the sucrose diet. When the rats were fed fructose, the fatal organ abnormalities occured.
Lysl oxidase is a copper-dependent enzyme that participates in the formation of collagen and elastin. Fructose seems to interfere with copper metabolism to such an extent that collagen and elastin cannot form in growing animals--hence the hypertrophy of the heart and liver in young males. The females did not develop these abnormalities, but they resorbed their litters.1
These experiements should give us pause when we consider the great increase in the use of high fructose corn syrup during the past 30 years, particularly in soft drinks, fruit juices and other beverages aimed at growing children, children increasingly likely to be copper deficient as modern parents no longer serve liver to their families. (Liver is by far the best source of copper in human diets.)
"The bodies of the children I see today are mush," observed a concerned chiropractor recently. The culprit is the modern diet, high in fructose and low in copper-containing foods, resulting in inadequate formation of elastin and collagen--the sinews that hold the body together.
BINGEING ON FRUCTOSE
Until the 1970s most of the sugar we ate came from sucrose derived from sugar beets or sugar cane. Then sugar from corn--corn syrup, fructose, dextrose, dextrine and especially high fructose corn syrup (HFCS)--began to gain popularity as a sweetener because it was much less expensive to produce. High fructose corn syrup can be manipulated to contain equal amounts of fructose and glucose, or up to 80 percent fructose and 20 percent glucose.2 Thus, with almost twice the fructose, HFCS delivers a double danger compared to sugar.
(With regards to fruit, the ratio is usually 50 percent glucose and 50 percent fructose, but most commercial fruit juices have HFCS added. Fruit contains fiber which slows down the metabolism of fructose and other sugars, but the fructose in HFCS is absorbed very quickly.)
In 1980 the average person ate 39 pounds of fructose and 84 pounds of sucrose. In 1994 the average person ate 66 pounds of sucrose and 83 pounds of fructose, providing 19 percent of total caloric energy.3 Today approximately 25 percent of our average caloric intake comes from sugars, with the larger fraction as fructose.4
High fructose corn syrup is extremely soluble and mixes well in many foods. It is cheap to produce, sweet and easy to store. It’s used in everything from bread to pasta sauces to bacon to beer as well as in "health products" like protein bars and "natural" sodas.
FRUCTOSE FOR DIABETICS?
In the past, fructose was considered beneficial to diabetics because it is absorbed only 40 percent as quickly as glucose and causes only a modest rise in blood sugar.5 However, research on other hormonal factors suggests that fructose actually promotes disease more readily than glucose. Glucose is metabolized in every cell in the body but all fructose must be metabolized in the liver.6 The livers of test animals fed large amounts of fructose develop fatty deposits and cirrhosis, similar to problems that develop in the livers of alcoholics.
Pure fructose contains no enzymes, vitamins or minerals and robs the body of its micronutrient treasures in order to assimilate itself for physiological use.7 While naturally occurring sugars, as well as sucrose, contain fructose bound to other sugars, high fructose corn syrup contains a good deal of "free" or unbound fructose. Research indicates that this free fructose interferes with the heart’s use of key minerals like magnesium, copper and chromium. Among other consequences, HFCS has been implicated in elevated blood cholesterol levels and the creation of blood clots. It has been found to inhibit the action of white blood cells so that they are unable to defend the body against harmful foreign invaders.8
Studies on the Maillard reaction indicate that fructose may contribute to diabetic complications more readily than glucose. The Maillard reaction is a browning reaction that occurs when compounds are exposed to various sugars. Fructose browns food seven times faster than glucose, resulting in a decrease in protein quality and a toxicity of protein in the body.9 This is due to the loss of amino acid residues and decreased protein digestibility. Maillard products can inhibit the uptake and metabolism of free amino acids and other nutrients such as zinc, and some advanced Maillard products have mutagenic and/or carcinogenic properties. The Maillard reactions between proteins and fructose, glucose, and other sugars may play a role in aging and in some clinical complications of diabetes.10
Fructose reduces the affinity of insulin for its receptor, which is the hallmark of type-2 diabetes. This is the first step for glucose to enter a cell and be metabolized. As a result, the body needs to pump out more insulin to handle the same amount of glucose.21
Nancy Appleton, PhD, clinical nutritionist, has compiled a list of the harmful effects of fructose in her books Lick the Sugar Habit, Healthy Bones, Heal Yourself With Natural Foods, The Curse Of Louis Pasteur and Lick the Sugar Habit Sugar Counter. She points out that consumption of fructose causes a significant increase in the concentration of uric acid; after ingestion of glucose, no significant change occurs. An increase in uric acid can be an indicator of heart disease.12 Furthermore, fructose ingestion in humans results in increases in blood lactic acid, especially in patients with preexisting acidotic conditions such as diabetes, postoperative stress or uremia. Extreme elevations cause metabolic acidosis and can result in death.13
Fructose is absorbed primarily in the jejunum before metabolism in the liver. Fructose is converted to fatty acids by the liver at a greater rate than is glucose.14 When consumed in excess of dietary glucose, the liver cannot convert all of the excess fructose in the system and it may be malabsorbed. The portion that escapes conversion may be thrown out in the urine. Diarrhea can be a consequence.19 A study of 25 patients with functional bowel disease showed that pronounced gastrointestinal distress may be provoked by malabsorption of small amounts of fructose.26
Fructose interacts with oral contraceptives and elevates insulin levels in women on "the pill."17
In studies with rats, fructose consistently produces higher kidney calcium concentrations than glucose. Fructose generally induces greater urinary concentrations of phosphorus and magnesium and lowered urinary pH compared with glucose.18
In humans, fructose feeding leads to mineral losses, especially higher fecal excretions of iron and magnesium, than did subjects fed sucrose. Iron, magnesium, calcium, and zinc balances tended to be more negative during the fructose-feeding period as compared to balances during the sucrose-feeding period.19
There is significant evidence that high sucrose diets may alter intracellular metabolism, which in turn facilitates accelerated aging through oxidative damage. Scientists found that the rats given fructose had more undesirable cross-linking changes in the collagen of their skin than in the other groups. These changes are also thought to be markers for aging. The scientists say that it is the fructose molecule in the sucrose, not the glucose, that plays the larger part.20
Because it is metabolized by the liver, fructose does not cause the pancreas to release insulin the way it normally does. Fructose converts to fat more than any other sugar. This may be one of the reasons Americans continue to get fatter. Fructose raises serum triglycerides significantly. As a left-handed sugar, fructose digestion is very low. For complete internal conversion of fructose into glucose and acetates, it must rob ATP energy stores from the liver.21
Not only does fructose have more damaging effects in the presence of copper deficiency, fructose also inhibits copper metabolism--another example of the sweeteners double-whammy effect. A deficiency in copper leads to bone fragility, anemia, defects of the connective tissue, arteries, and bone, infertility, heart arrhythmias, high cholesterol levels, heart attacks, and an inability to control blood sugar levels.22
Although these studies were not designed to test the effects of fructose on weight gain, the observation of increased body weight associated with fructose ingestion is of interest. One explanation for this observation could be that fructose ingestion did not increase the production of two hormones, insulin and leptin, that have key roles in the long-term regulation of food intake and energy expenditure.23
The magnitude of the deleterious effects of fructose varies depending on such factors as age, sex, baseline glucose, insulin, triglyceride concentrations, the presence of insulin resistance, and the amount of dietary fructose consumed.24 Some people are more sensitive to fructose. They include hypertensive, hyperinsulinemic, hypertriglyceridemic, non-insulin dependent diabetic people, people with functional bowel disease and postmenopausal women.25
Everyone should avoid over-exposure to fructose, but especially those listed above. One or two pieces of fruit per day is fine, but commercial fruit juices and any products containing high fructose corn syrup aremore dangerous than sugar and should be removed from the diet.
1. Fields, M, Proceedings of the Society of Experimental Biology and Medicine, 1984, 175:530-537.
2. Appleton, Nancy, PhD, Fructose is No Answer For a Sweetener, http://www.mercola.com/2002/jan/5/fructose.htm.
3. Beatrice Trum Hunter, Confusing Consumers About Sugar Intake, Consumer’s Research 78, no 1 (January 1995): 14-17.
4. Fallon, Sally and Mary Enig, Nourishing Traditions, New Trends Publishing, Washington DC, 2001, p. 23.
5. Hallfrisch, Judith, Metabolic Effects of Dietary Fructose, FASEB Journal 4 (June 1990): 2652-2660.
6. American Journal of Clinical Nutrition, November 2002 Vol. 76, No. 5, 911-922.
7. Appleton, Nancy Ph.D., Fructose is No Answer For a Sweetener, http://www.mercola.com/2002/jan/5/fructose.htm.
9. H. F. Bunn and P. J. Higgins, Reaction of Nonosaccharides with Proteins; Possible Evolutionary Significance, Science 213 (1981):2222-2244.
10. William L Dills Jr., Protein Fructosylation: Fructose and the Maillard Reaction, American Journal of Clinical Nutrition 58 (suppl) (1993): 779S-787S.
12. J. MacDonald, Anne Keyser, and Deborah Pacy, Some Effects, in Man, of Varying the Load of Glucose, Sucrose, Fructose, or Sorbitol on Various Metabolites in Blood, American Journal of Clinical Nutrition 31 (August 1978)): 1305-1311.
13. Hallfrisch, Judith, Metabolic Effects of Dietary Fructose, FASEB Journal 4 (June 1990): 2652-2660.
14. D. Zakim and R. H. Herman, Fructose Metabolism II, American Journal of Clinical Nutrition 21: 315-319, 1968.
15. A. E. Bender and K. B. Damji, Some Effects of Dietary Sucrose, World Review of Nutrition and Dietetics 15 (1972): 104-155.
16. J. J. Rumessen and E. Gudmand-Hoyer, Functional Bowel Disease: Malabsorption and Abdominal Distress After Ingestion of Fructose, Sorbitol, and Fructose-Sorbitol Mixtures, Gastroenterology 95, no. 3 (September 1988): 694-700.
17. Hunter,Beatrice Trum,Confusing Consumers About Sugar Intake, Consumers’ Research 78, no 1 (January 1995): 14-17.
18. A. E. Bergstra, A. G. Lemmens, and A. C. Beynens, Dietary Fructose vs. Glucose Stimulates Nephrocalcinogenesis in Female Rats, Journal of Nutrition 123, no. 7 (July 1993): 1320-1327.
19. R. Ivaturi and C. Kies, Mineral Balances in Humans as Affected by Fructose, High Fructose Corn Syrup and Sucrose, Plant Foods for Human Nutrition 42, no. 2 (1992): 143-151.
20. Roger B. Mc Donald, Influence of Dietary Sucrose on Biological Aging, American Journal of Clinical Nutrition 62 (suppl), (1995): 284s-293s.
21. H. Hallfrisch, et al.,The Effects of Fructose on Blood Lipid Levels, American Journal of Clinical Nutrition, 37: 5, 1983, 740-748.
22. Klevay, Leslie, Acting Director of the U.S. Agriculture Department’s Human Nutrition Research Center, Grand Forks, N.D.
23. Observation by Nancy Appleton, PhD.
24. Hollenbeck, Claire B., Dietary Fructose Effects on Lipoprotein Metabolism and Risk for Coronary Artery Disease, American Journal of Clinical Nutrition 58 (suppl), (1993): 800S-807S.
25. Appleton, Nancy Ph.D., Fructose is No Answer For a Sweetener, http://www.mercola.com/2002/jan/5/fructose.htm.
Interesting read Eric. Thanks.
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