Science Explains How Fructose, Glucose Affect Our Appetite

Scientists have revealed how fructose and glucose have different effects on physiological and behavioral responses to food.

To assess the different effects of the two sugars on hunger and food cue responses in the brain, Kathleen A. Page and colleagues conducted fMRI scans on 24 people who had been given drinks sweetened with fructose on one day and glucose on another day.

Participants were shown images of high-calorie foods and then reported their level of hunger and desire for the foods. Participants reported greater hunger and exhibited greater activity in the orbitofrontal cortex and visual cortex of the brain in response to the food images after ingesting fructose, compared with responses after ingesting glucose.

Further, the authors found that fructose produced a smaller plasma insulin response than glucose. When presented with a choice between delayed monetary rewards or immediate high-calorie food rewards, participants displayed greater willingness to give up monetary rewards for food rewards after ingesting fructose than after ingesting glucose. The results suggest that ingestion of fructose may not produce the same satiety effects as glucose, according to the authors.

Due to differences in metabolism, fructose may enhance the reward value of high-calorie food and promote eating, compared with glucose. (ANI)

Diabetes debate: HbA1c or glucose?

If it were a boxing match, the debate over whether hemoglobinshould be used to diagnose diabetes would place the odds-on favorite in the “Yes” corner. In the “No” corner would be the underdog. At least based on the mainstream consensus since 2010, HbA1c for diagnosis is well established as an alternative to measuring glucose.

At the July 2013 meeting of the American Association for Clinical Chemistry, where opposing sides on this question squared off in a debate, a quick vote beforehand showed “Yes” with a 20-to-one edge. But the speakers came armed with provocative data on comparative benefits and drawbacks, and both sides scored solid points.

Most of the debate centered on two questions: Which is more accurate, HbA1c or glucose? And with regard to diagnosing diabetes and predicting risk of complications, what are the most important things to measure anyway?

“Even though we’ve been measuring glucose in blood for 100 years, the question that comes up is: How accurate is a glucose result?” said moderator David Sacks, MB, ChB, FRCPath, senior investigator with the National Institutes of Health, in introductory remarks before the debate.

Dr. Sacks

Dr. Sacks

Not only is there the usual preanalytical and analytical variation, but there is also large biological variability among people and even within a single person, he pointed out. “That means for every one of you sitting here, if you are healthy, your fasting plasma glucose can have a coefficient of variation of up to 8.3 percent between today and tomorrow, even if everything’s the same.”

HbA1c is not a perfect alternative, but since 1993, when the NGSP (formerly the National Glycohemoglobin Standardization Program) launched efforts to standardize HbA1c, there has been a huge improvement in the assay, Dr. Sacks said. “The means are much closer to the target, and the standard deviations have been reduced considerably. So while HbA1c is not perfect, it’s getting progressively better over time.”

In Dr. Sacks’ view, there are substantial deficiencies in the glucose criteria for diagnosing diabetes. Hemoglobin A1c standardization has significantly improved the measure. “Of course there are deficiencies in hemoglobin A1c. But hemoglobin A1c can be measured accurately in the vast majority of subjects with hemoglobin variants.”

The FDA’s approval of Roche’s Tina-quant HbA1c Dx blood test last spring showed just how far the HbA1c assay has come, said Robert A. Vigersky, MD, director of the Diabetes Institute at Walter Reed National Military Medical Center. In contrast with coefficients of variation typical of HbA1c 20 years ago, “the coefficient of variation in this assay was 1.5 percent. And I think that actually makes a very good case for the use of HbA1c for diagnosis, because it has by far the least analytic variability or overall variability.”

The American Diabetes Association made a big shift in 1997 when it lowered the recommended cut point for diagnosing diabetes. “If you have a fasting plasma glucose of 126 mg/dL or greater, you have diabetes. And prior to 1997, it had been 140. And the reason for that change was that it became obvious from the data that complications, particularly the microvascular complications like retinopathy and nephropathy, were appearing in people who had blood sugars much lower than 140.”

Dr. Vigersky

Dr. Vigersky

Still, Dr. Vigersky said, the variability of fasting glucose is high. “Of all the tests, the oral glucose tolerance test has the most variability, besides which it’s the most cumbersome to perform and our patients don’t like doing it.”

What are the implications of this lack of reproducibility? He pointed to a Swedish study of 2,200 women of whom 241 were diagnosed as having diabetes based on the oral glucose tolerance test. But when the test was repeated, 19 percent of them had normal glucose tolerance, 32 percent had impaired glucose tolerance, and only 49 percent had the diagnosis confirmed.

Findings like these were what led the American Diabetes Association to convene an International Expert Committee in 2009 to weigh whether HbA1c should be used for diagnosing diabetes. “They came down on the side of yes.” In 2010, the ADA added an HbA1c of 6.5 percent or greater as a diagnostic cut point.

“And needless to say, this wasn’t accepted by everyone, and we’re still having this debate four years later,” Dr. Vigersky pointed out. But he thinks it’s significant that when the recommendation to use HbA1c for diagnosis was adopted, the typical CV was much higher than it is now. “This new FDA approval is such a game changer for the field, because we now have an assay that when the CVs were 10 percent the International Expert Committee already thought it was acceptable to use, and now we’re down to a real CV of 1.5 percent.”

The diagnosis of diabetes is very different depending on which parameter you use, Dr. Vigersky said. The reason: “We’re measuring very different aspects of dysglycemia.” On a Venn diagram showing prevalence of diabetes by different measures, the largest circle would be the two-hour post-glucose load and the smallest would be the circle of HbA1c.

How many people have diabetes, diagnosed or undiagnosed? “By fasting plasma glucose of 126 there are 21.5 million people based on the latest data from 2005–2006. Using just HbA1c, there would be fewer. If you used either glucose or HbA1c, there would be 22.4 million. If you used fasting plasma glucose or a glucose tolerance test there would be more. So depending on the diagnostic criteria, there are somewhere between 20 and 27 million people in the U.S. who have diabetes.”

Depending on what you want to believe, “you might want to pick, for political reasons, the criterion that gives you the highest number of people,” Dr. Vigersky said. “And I’ve heard people in important places say they’ll be damned if they’ll allow criteria to exist that show there are fewer people with diabetes.”

Interestingly, the data show a much greater increase in the prevalence of diabetes based on HbA1c over the past 10 years compared with fasting plasma glucose, he said. “In the diagnosis of prediabetes, if you have the cut point of an HbA1c of 5.7, in 1999 the prevalence was 10 percent and now the prevalence is almost 20 percent, almost a doubling in the last decade of prediabetes based on HbA1c.”

“But prediabetes affected 25 percent of the population if you used fasting glucose in 1999–2000 and only a slight increase to now—27.5 percent. So we’re measuring different things. We’re measuring the pathophysiology of a different aspect of dysglycemia when we throw in the HbA1c as a measure for the diagnostic criteria.”

It’s true that glycation rates affect interpretation of HbA1c, Dr. Vigersky said. Studies have shown for a mean glucose over a three-month period, “there’s a significant splay in the data of HbA1cs. And I think you would conclude that some people are high glycators and some people are low glycators at the same blood glucose levels.”

But these differences have important implications, he pointed out. “If you look at the complications of retinopathy and nephropathy, those with high glycation rates had much higher percentages, by a factor of six, compared to those with low glycation rates. So I would argue that even if we understand that there’s biologic variability and genetic variability in glycation rates, it may be beneficial to overestimate and pick up those with high glycation rates, because they in fact are at most risk of developing complications of diabetes.”

A powerful study (Selvin E, et al. Glycated hemoglobin, diabetes, and cardiovascular risk in nondiabetic adults. N Engl J Med. 2010; 362:800–811) looked at the prognostic value of HbA1c and fasting glucose done in patients during 1990–1992 and did a followup in 2010, some 20 years later, to see which of these two parameters, HbA1c or fasting glucose, might be more predictive of cardiovascular events and death. “And it turns out that fasting glucose was not predictive at all in patients without diabetes,” Dr. Vigersky said.

“If you had a fasting glucose in the prediabetes range of 100 to 125 mg/dL, it had no predictive value for coronary heart disease. But if you had an HbA1c between six and 6.4 percent, you had an 88 percent risk of developing coronary heart disease. Similar effects were found in comparing HbA1c with glucose for ischemic stroke and all-cause mortality. “So does HbA1c predict cardiovascular disease as well as glucose? I’d say actually better, since it reflects other aspects of dysglycemia.”

In Dr. Vigersky’s view, the advantages of HbA1c in diagnosing diabetes are many. “Biochemically, it has greater analytic accuracy and better reproducibility. Clinically, it’s more convenient and fasting isn’t required, and there is less day-to-day variation during periods of stress and illness. Epidemiologically, it’s a better predictor of cardiovascular events and death than fasting. And there are some interesting pathophysiologic aspects related to the different glycation rates that may better predict complications.”

In conclusion, he said, “I would say that HbA1c should be used to diagnose diabetes. But—and this may need to be modified going forward—if you only use an HbA1c it should be seven percent or greater, or in combination with a fasting glucose of 126 or greater if the HbA1c is between 6.5 and 6.9.”

“Should hemoglobin A1c be used to diagnose diabetes? I would answer no to that question,” said William Herman, MD, MPH, director of the Michigan Center for Diabetes Translational Research, in staking out his position in the debate.

He agreed that HbA1c has advantages. “HbA1c is certainly convenient. It can be drawn anytime. It’s less susceptible to short-term lifestyle modification. Patients are not going to game you or, if they fast for three days before their appointment, will not fool you in terms of their average level of glycemia. Compared to glucose, HbA1c certainly has a smaller intra-individual biologic variation with about a four percent coefficient of variation, and it has benefited tremendously from international assay standardization.”

“But HbA1c has a major disadvantage for diagnosis of diabetes, and that is the potential for bias that consistently lowers or raises the measured HbA1c value relative to the true level of glycemia.” It’s a systematic error, he added, and it creates the most problem in the near-normal glucose range.

Many factors may alter hemoglobin A1c test results—for example, hemoglobinopathies, thalassemia syndromes, or decreased red cell age—and the recommendation is that if the patient has any of these factors, either a different assay or an alternative measure of glycemia should be used, Dr. Herman said. But possibly more problematic may be the less well-known factors that may alter HbA1c results.

If the patient has uremia, hyperbilirubinemia due to liver failure, iron deficiency—which occurs in about 20 percent of women of reproductive age—excessive use of vitamin C and vitamin E, hypertriglyceridemia, or excessive use of opiates, “these can affect the accuracy of HbA1c, and if you know about them you can use an alternative measure,” he said. “But if you don’t know about them, you may be fooled by the HbA1c test result. And if that’s not bad enough, there are a number of yet unknown factors that may alter HbA1c levels relative to the true level of glycemia.”

He believes the push to use HbA1c to diagnose diabetes has to do with familiarity bias and ambiguity aversion. “Clinicians are used to using HbA1c to monitor glycemic control in patients with established diabetes, and they question, well, why not just use the same test for the diagnosis? But I think this puts us on a slippery slope.”

The problem he sees is that at the lower end of the HbA1c range, which is where the diagnostic numbers are, HbA1c levels vary considerably among individuals, but within individuals they change little over time. Only about one-third of the variance in HbA1c can be explained on the basis of measures of glycemia.

“Glucose is glucose, yet an HbA1c of 6.5 corresponds to very different average glucose levels across individuals. So why may HbA1c not be an accurate measure of glycemia? I think to answer this, one needs to think of the ration-ale or the assumptions we make as to why HbA1c is a good measure of glycemia,” Dr. Herman said.

It’s commonly assumed that, first, erythrocyte lifespan is constant; second, erythrocytes are freely permeable to glucose; and third, HbA1c is formed slowly and nonenzymatically. But studies have shown all three of those assumptions may not be true, he said. “In the hematologically normal population, mean red cell age has been found to be about 50 days, but there is physiologic variation from about 40 days to 60 days. And if one looks at the impact of a 10-day shorter mean red cell age, it will in fact lower HbA1c about one point.”

Hemoglobin lives in the intracellular environment, while glucose is in the extracellular environment, Dr. Herman said. “The differences between intracellular and extracellular measures of glycemia are common in clinical practice and largely unexplained. This difference is measured as the glycation gap, and within individuals it is a characteristic of the individual and is stable over time.”

Interestingly, he added, there seems to be high heritability of glycation gap in nondiabetic twins. “If one twin has a high glycation gap, the other does too, and this leads us into the question of genetics. Here, I think the data are showing associations between genetic polymorphisms and hemoglobin glycation independent of glycemia.”

As people age, there’s very little change in fasting glucose, very little change in fructosamine, but a largely unexplained increase in HbA1c, such that older people have higher HbA1c levels than younger people. Smoking appears to affect hemoglobin glycation, alcohol consumption seems to affect it inversely (lifelong abstainers have HbA1c levels .41 percent higher than people who have three or more drinks a day), and an increase in total daily energy intake from dietary fat is associated with an increase in HbA1c, Dr. Herman said.

“In addition, there are well-described racial and ethnic differences in hemoglobin A1c. There is a consistently higher HbA1c in racial and ethnic minority groups compared with whites, despite identical glucose profiles. So we come then to the question, should hemoglobin A1c be used to diagnose diabetes?”

“If the clinical laboratory-based hemoglobin A1c assay—not a point-of-care assay—is available, it could be performed. Or if the glucose testing is not convenient. If you have a high index of suspicion and a patient is coming after lunch for a visit, then sure, do a hemoglobin A1c level,” Dr. Herman advised. “But if you’re suspicious of type 1 diabetes with a relatively recent onset of severe hyperglycemia, then HbA1c testing is not appropriate. You’re certainly much better off measuring glucose, and you can measure HbA1c when there are no known patient factors that preclude interpretation of the HbA1c.”

He would argue, however, that that is almost never. “As we’ve already pointed out, there are a number of patient factors that preclude the interpretation of hemoglobin A1c. And I would argue that most clinicians screening a patient for type 2 diabetes are not going to know when these things are going on. You certainly could do a hemoglobin electrophoresis and a complete blood count, do a reticulocyte count, do a stool guaiac for blood loss, do a BUN-creatinine-liver function study, a lipid profile, iron studies, drug screens, and assess all of these other factors, and do your hemoglobin A1c and feel relatively confident that it’s accurate.”

“But if you don’t want to do those things, you could also consider measuring a glucose level. If hemoglobin A1c is measured without glucose, undetected, systematic bias may exist and repeated measurements of hemoglobin A1c will not reveal the true level of glycemia. If an individual has low-grade hemolysis and the clinician keeps measuring hemoglobin A1c, it’s always going to be low. If glucose is measured, random error may occur, but repeated measurements will reveal the true level of glycemia,” Dr. Herman said.

An audience member asked Dr. Herman why he was so confident in the ability of the laboratory to measure glucose accurately, given all the problems of getting specimens to the lab, and standardization issues involving whole blood versus plasma. Dr. Herman conceded the point. “It’s true—I’ve seen tubes sitting out on desktops for hours waiting to get transported to the labs. And these are all real issues. But they are addressable issues as well, and I’d like to see us spend as much effort on that as we’ve spent on hemoglobin A1c standardization.”

His conclusion: “Hemoglobin A1c is potentially a systematically biased measure of glycemia, particularly in the near-normal range. Some reasons are known; some reasons remain unknown. And glucose may be less precise, but it is certainly an unbiased measure of glycemia and remains the preferred diagnostic test.”

In the end, the debate over HbA1c versus glucose couldn’t be said to produce a knockout, a split decision, or a draw. Unlike a prizefight, this debate will go into overtime. When Dr. Sacks polled the audience again, clearly a few had been convinced to switch to “no on HbA1c.” But the majority were still proponents—leaving plenty of grounds for a reprise of the HbA1c debate, which the AACC and the Endocrine Society plan to hold at this year’s meeting in July.

‘Sugar gel’ helps premature babies.

A dose of sugar given as a gel rubbed into the inside of the cheek is a cheap and effective way to protect premature babies against brain damage, say experts.

premature baby

Dangerously low blood sugar affects about one in 10 babies born too early. Untreated, it can cause permanent harm.

Researchers from New Zealand tested the gel therapy in 242 babies under their care and, based on the results, say it should now be a first-line treatment.

Their work is published in The Lancet.

Sugar dose

Dextrose gel treatment costs just over £1 per baby and is simpler to administer than glucose via a drip, say Prof Jane Harding and her team at the University of Auckland.

“Start Quote

This is a cost effective treatment and could reduce admissions to intensive care services which are already working at high capacity levels”

Andy Cole Bliss

Current treatment typically involves extra feeding and repeated blood tests to measure blood sugar levels.

But many babies are admitted to intensive care and given intravenous glucose because their blood sugar remains low – a condition doctors call hypoglycaemia.

The study assessed whether treatment with dextrose gel was more effective than feeding alone at reversing hypoglycaemia.

Neil Marlow, from the Institute for Women’s Health at University College London, said that although dextrose gel had fallen into disuse, these findings suggested it should be resurrected as a treatment.

We now had high-quality evidence that it was of value, he said.

Andy Cole, chief executive of premature baby charity Bliss, said: “This is a very interesting piece of new research and we always welcome anything that has the potential to improve outcomes for babies born premature or sick.

“This is a cost-effective treatment and could reduce admissions to intensive care services, which are already working at high capacity levels.

“While the early results of this research show benefits to babies born with low blood sugars, it is clear there is more research to be done to implement this treatment.”

Brain may play key role in blood sugar metabolism and diabetes development.

A growing body of evidence suggests that the brain plays a key role in glucose regulation and the development of type 2 diabetes, researchers write in the Nov. 7 ssue of the journal Nature. If the hypothesis is correct, it may open the door to entirely new ways to prevent and treat this disease, which is projected to affect one in three adults in the United States by 2050.

In the paper, lead author Dr. Michael W. Schwartz, UW professor of medicine and director of the Diabetes and Obesity Center of Excellence, and his colleagues from the universities of Cincinnati, Michigan, and Munich,  note that the brain was originally thought to play an important role in maintaining normal glucose metabolism  With the discovery of insulin in the 1920s, the focus of research and diabetes care shifted to almost exclusively to insulin. Today, almost all treatments for diabetes seek to either increase insulin levels or increase the body’s sensitivity to insulin.

“These drugs,” the researchers write, “enjoy wide use and are effective in controlling hyperglycemia [high blood sugar levels], the hallmark of type 2 diabetes, but they address the consequence of diabetes more than the underlying causes, and thus control rather than cure the disease.”

New research, they write, suggests that normal glucose regulation depends on a partnership between the insulin-producing cells of the pancreas, the pancreatic islet cells, and neuronal circuits in the hypothalamus and other brain areas that are intimately involved in maintaining normal glucose levels. The development of diabetes type 2, the authors argue, requires a failure of both the islet-cell system and this brain-centered system for regulating blood sugar levels .

In their paper, the researchers review both animal and human studies that indicate the powerful effect this brain-centered regulatory system has on blood glucose levels independent of the action of insulin. One such mechanism by which the system promotes glucose uptake by tissues is by stimulating what is called “glucose effectiveness.” As this process accounts for almost 50 percent of normal glucose uptake, it rivals the impact of insulin-dependent mechanisms driven by the islet cells in the pancreas.

The findings lead the researchers to propose a two-system model of regulating blood sugar levels composed of the islet-cell system, which responds to a rise in glucose levels by primarily by releasing insulin, and the brain-centered system that enhances insulin-mediated glucose metabolism while also stimulating glucose effectiveness.

The development of type 2 diabetes appears to involve the failure of both systems, the researchers say. Impairment of the brain-centered system is common, and it places an increased burden on the islet-centered system. For a time, the islet-centered system can compensate, but if it begins to fail, the brain-centered system may decompensate further, causing a vicious cycle that ends in diabetes.

Boosting insulin levels alone will lower glucose levels, but only addresses half the problem. To restore normal glucose regulation requires addressing the failures of the brain-centered system as well. Approaches that target both systems may not only achieve better blood glucose control, but could actually cause diabetes to go into remission, they write.

Measuring Blood Sugar With Light.

Technology designed in Germany may help people with Type 1 and Type 2 diabetes; described in Review of Scientific Instruments

WASHINGTON D.C. October 25, 2013 — One of the keys to healthful living with Type 1 and Type 2 diabetes is monitoring blood glucose (sugar) levels to ensure they remain at stable levels. People can easily and reliably do this at home using electronic devices that read sugar levels in a tiny drop of blood.

Now a team of German researchers has devised a novel, non-invasive way to make monitoring easier. Using infrared laser light applied on top of the skin, they measure sugar levels in the fluid in and under skin cells to read blood sugar levels. They describe their method in the current edition of Review of Scientific Instruments, which is produced by AIP Publishing.

“This opens the fantastic possibility that diabetes patients might be able to measure their glucose level without pricking and without test strips,” said lead researcher, Werner Mäntele, Ph.D. of Frankfurt’s Institut für Biophysik, Johann Wolfgang Goethe-Universität.

“Our goal is to devise an easier, more reliable and in the long-run, cheaper way to monitor blood glucose,” he added.

The “Sweet Melody” of Glucose

Their new optical approach uses photoacoustic spectroscopy (PAS) to measure glucose by its mid-infrared absorption of light. A painless pulse of laser light applied externally to the skin is absorbed by glucose molecules and creates a measurable sound signature that Dr. Mäntele’s team refers to as “the sweet melody of glucose.” This signal enables researchers to detect glucose in skin fluids in seconds.

The data showing the skin cell glucose levels at one-hundredth of a millimeter beneath the skin is related to blood glucose levels, Mäntele said, but previous attempts to use PAS in this manner have been hampered by distortion related to changes of air pressure, temperature and humidity caused by the contact with living skin.

To overcome these constraints, the team devised a design innovation of an open, windowless cell architecture. While it is still experimental and would have to be tested and approved by regulatory agencies before becoming commercially available, the team continues to refine it.

Is Fructose As Addictive As Alcohol?

Fructose, which literally means “fruit sugar,”* sounds so sweet and innocent. And indeed, when incorporated into the diet in moderate amounts in the form of fruit – always organic and raw, when possible – it’s about as pure and wholesome as as a nutrient can get.

Toxic Fructose Addiction: The 800 Ounce Gorilla In The Room

Not so for industrially processed fructose in isolate form, which may be as addictive as alcohol,[i] and perhaps even morphine [ii] [iii]and which according to USDA research published in 2008 into major trends in U.S. food consumption patterns, 1970-2005, we now consume at the rate of at least 50 lbs a year — the ‘800 ounce gorilla’ in the room.[iv]

Our dietary exposure to fructose, of course, is primarily through either sugar (sucrose), which is a disaccharide comprised of 50% fructose and 50% glucose by weight, or through high-fructose corn syrup (HFCS), which is mostly a 55% fructose and 45% glucose blend of monosaccharides, but goes as high as 90% fructose and 10% glucose in HFCS-90 form.  Pasteurized fruit juices are another concentrated source of fructose, but increasingly even pasteurized fruit juice is being adulterated with additional sugar or HFCS for reasons that have mostly to do with protecting the manufacturer’s bottom line.

Because high-fructose corn syrup contains free-form monosaccharides of fructose and glucose, it cannot be considered biologically equivalent to sucrose, which has a glycosidic bond that links the fructose and glucose together, and which slows its break down in the body. The attempt by the HFCS industry to re-label their product as “corn sugar,” which was recently denied by the FDA,[v] belies their anxiety about the differences, and also reveals growing awareness among the public of isolated fructose’s inherently toxic properties.

The reality is that fructose can cause far more damage than glucose, and we must look beyond caloric equivalences to understand this. While in times of need (e.g. starvation, post-workout glycogen depletion), fructose is as effective as glucose in replenishing glycogen stores, in “hypercaloric” states of excess consumption, it can lead to a process known as glycation whereby a sugar binds with protein or lipid molecules, often resulting in damage to cells and tissues.

For example, in vitro studies show that fructose damages proteins seven times more rapidily than glucose through a process known as protein fructosylation, which is when a sugar undergoes a Malliard reaction with a protein, which basically results in the caramelization (browing) of blood and tissue contents, “gumming up the works.” For example, if you try baking a pastry made with fructose, instead of white sugar, it will brown much more rapidly as a result of this Malliard reactivity.

Fructose actually shares great resemblance to alcohol (ethanol), such as being capable of stimulating dopamine production in our brain, as well as sharing similar metabolic pathways and effects on the liver (e.g. fatty liver). Their great similarities make even more sense when you consider that fructose can easily be converted into ethanol with a pinch of yeast in order to make alcoholic beverages.

So toxic is “purified” fructose that here at GreenMedInfo we have indexed research on over 70 adverse health effects associated with its excessive consumption, which include:

  • Insulin Resistance (32 studies)
  • Fatty Liver (22 studies)
  • Obesity (13 studies)
  • Metabolic Syndrome (19 studies)
  • Hypertension (10 studies)
  • Elevated Uric Acid (9 studies)
  • Elevated Triglycerides (14 studies)
  • Belly Fat (2 studies)
  • Cardiovascular Diseases (4 studies)
  • Liver Stress (6 studies)
  • Pancreatic Cancer (2 studies)
  • Leptin Resistance (2 studies)

To view the first hand research on 70+ forms of fructose toxicity click the hyperlink.

Like many foods consumed en masse, which may have a lesser known dark side (e.g. wheat), our global fixation on fructose may reveal something about it’s hitherto under appreciated addictive properties.

Fructose’s Drug-like Hold On Our Bodies 

Fructose addiction and alcoholism, in fact, share a number of parallels. In an article titled, “Fructose: metabolic, hedonic, and societal parallels with ethanol,” published in the Journal of the American Dietetic Association in 2010, Robert H. Lustig, MD broke new ground by identifying the great similarities between these two substances.

Rates of fructose consumption continue to rise nationwide and have been linked to rising rates of obesity, type 2 diabetes, and metabolic syndrome. Because obesity has been equated with addiction, and because of their evolutionary commonalities, we chose to examine the metabolic, hedonic, and societal similarities between fructose and its fermentation byproduct ethanol. Elucidation of fructose metabolism in liver and fructose action in brain demonstrate three parallelisms with ethanol. First, hepatic fructose metabolism is similar to ethanol, as they both serve as substrates for de novo lipogenesis, and in the process both promote hepatic insulin resistance, dyslipidemia, and hepatic steatosis. Second, fructosylation of proteins with resultant superoxide formation can result in hepatic inflammation similar to acetaldehyde, an intermediary metabolite of ethanol. Lastly, by stimulating the “hedonic pathway” of the brain both directly and indirectly, fructose creates habituation, and possibly dependence; also paralleling ethanol. Thus, fructose induces alterations in both hepatic metabolism and central nervous system energy signaling, leading to a “vicious cycle” of excessive consumption and disease consistent with metabolic syndrome. On a societal level, the treatment of fructose as a commodity exhibits market similarities to ethanol. Analogous to ethanol, societal efforts to reduce fructose consumption will likely be necessary to combat the obesity epidemic.

While the parallel between fructose and alcohol consumption may seem strange, the intimate connection between what we eat and our psychological health is beginning to gain wider recognition, especially considering new research linking aggression to trans fatty acid consumption, episodes of acute wheat mania, and the widespread presence of opiates in common foods

It may come as a surprise to many, but there is a fructose-opiate infatuation deeply embedded within mammalian biology, which has been the subject of scientific investigation since the late 80’s. A study published in the European Journal of Pharmacology in 1988 found that both glucose and fructose were capable of antagonizing morphine-induced pain killing effects, likely due to the direct opioid effects of these sugars or their metabolic byproducts on the central nervous system. In fact, the researchers found that fructose was more potent than glucose in accomplishing these effects.

Could the narcotic properties of fructose, or one of its metabolic byproducts, explain why we would consume such vast quantities of something so inherently harmful to our bodies?

As it turns out, not only has fructose’s manifold toxic properties been studied, but researchers have also investigated what natural substances reduce fructose’s adverse effects.

GreenMedInfo contains research on 21 natural compounds with fructose toxicity attenuating action, including

·         Berberine

·         Fish Oil

·         Astaxanthin

·         Bitter Melon

·         Chlorella

·         Coconut Water

·         Garlic

·         Ginger

·         Holy Basil

·         Quinoa

·         Resveratrol

·         Spirulina

To view them all, you can visit our Fructose-Induced Toxicity page.

Ultimately, avoiding fructose in any other than its naturally embedded form in the intelligent and infinitely complex structures of food, e.g. fruit, is ideal. Food cravings for sweets, after all, may conceal unmet emotional or spiritual needs, so sometimes it is best to search deeper within for the answers. Or, using natural non- or low-calorie sweeteners like xylitol or steviamay also take the edge off an intense sweet tooth.

But, beyond the increasingly obvious adverse effects of isolated fructose to human health, is the “hidden” damage that fructose does to environmental/planetary health. This is because fructose from HFCS is invariably produced from genetically modified (GM) corn, which requires massive environmental inputs of harmful pesticides, glyphosate, gene products with the ability to transfer horizontally, and other unsustainable practices. The “hidden tax” of fructose consumption is the accelerating, GM-mediated destruction of the biosphere; a biosphere, mind you, without which human health and human existence, is not possible. 

*Fructose: derived from Latin fructus (“fruit”) + -ose (“sugar”).

[i] Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc. 2010 Sep ;110(9):1307-21.  

[ii] Antagonism of the morphine-induced locomotor activation of mice by fructose: comparison with other opiates and sugars, and sugar effects on brain morphine. Life Sci. 1991 ;49(10):727-34.

[iii] Antagonism of antinociception in mice by glucose and fructose: comparison of subcutaneous and intrathecal morphine. Eur J Pharmacol. 1988 Feb 9 ;146(2-3):337-40.

[iv] USDA Economic Research Service, Dietary Assessment of Major Trends in U.S. Food Consumption, 1970-2005

[v] Packaging Digest, FDA rejects renaming of high-fructose corn syrup, 6/7/2012


This is why high fructose corn syrup is dangerous.

High Fructose Corn Syrup, also known as HFCS, glucosefructose syrup, glucose syrup, fructose syrup, glucose/fructose, high-fructose maize syrup or corn sugar is a corn-based sweetener that is used in thousands of food products including sodas, soft drinks, fruit juices, ice cream, candy, baked goods, cookies, ketchup, soups, salad dressings, breads, crackers, etc.

HFCS is a mixture of fructose and glucose, and is used by food companies because it is cheaper than sugar and gives food products a longer shelf life.

HFCS is responsible for a host of health problems such as obesity, high cholesterol, insulin problems, Type 2 diabetes, liver damage, hypertension, high blood pressure, heart disease, cancer, migraines, ADHD, etc.
HFCS is often contaminated with mercury which can lead to brain damage.

Here is a great video about the dangers of HFCS:

Corn, the source of high fructose corn syrup, is now often genetically modified, which causes many serious health problems.

Glucose is used as fuel and metabolized by the cells in the body. In contrast, fructose can only be metabolized by the liver which turns fructose into fat. When consuming fructose, 30% will be stored as fat… Fructose, in contrast to glucose, has no effect on appetite, which results in overeating and obesity.

The fructose found in fruit and in some vegetables is actually quite healthy as it contains fiber, vitamins, minerals, enzymes and beneficial phytonutrients. In contrast, the fructose found in HFCS contains no nutrition and actually pulls nutrients from the body! HFCS hinders the absorption of minerals such as magnesium, copper and chromium and affects the receptors of insulin, leading to Type 2 diabetes. In addition, HFCS causes high cholesterol and impairs the immune system.

The food industry is trying to convince us that High Fructose Corn Syrup is natural, equal to sugar and therefore perfectly safe.

Do no longer believe the lies of the food industry and the ‘mainstream’ media. Contrary to what so-called ‘health experts’ claim, HFCS is not safe!

Avoid HFCS for 60 days and discover how your health will improve dramatically!

Other forms of fructose to avoid: crystalline fructose, chicory, inulin, iso glucose and Agave syrup, a highly processed sweetener that is nearly all-fructose.

Also avoid energy and sports drinks because they are loaded with sugar, chemical additives and artificial sweeteners.

Healthier HFCS alternatives:
Organic raw cane sugar, maple syrup, coconut nectar, palm sugar, raw honey and Stevia, the low calorie, all natural sweetener used in Paraguay for centuries.



‘Sugar gel’ helps premature babies

A dose of sugar given as a gel rubbed into the inside of the cheek is a cheap and effective way to protect premature babies against brain damage, say experts.

Dangerously low blood sugar affects about one in 10 babies born too early. Untreated, it can cause permanent harm.

Researchers from New Zealand tested the gel therapy in 242 babies under their care and, based on the results, say it should now be a first-line treatment.

Their work is published in The Lancet.

Sugar dose

Dextrose gel treatment costs just over £1 per baby and is simpler to administer than glucose via a drip, say Prof Jane Harding and her team at the University of Auckland.

 “Start Quote

This is a cost effective treatment and could reduce admissions to intensive care services which are already working at high capacity levels”

Andy ColeBliss

Current treatment typically involves extra feeding and repeated blood tests to measure blood sugar levels.

But many babies are admitted to intensive care and given intravenous glucose because their blood sugar remains low – a condition doctors call hypoglycaemia.

The study assessed whether treatment with dextrose gel was more effective than feeding alone at reversing hypoglycaemia.


Neil Marlow, from the Institute for Women’s Health at University College London, said that although dextrose gel had fallen into disuse, these findings suggested it should be resurrected as a treatment.

We now had high-quality evidence that it was of value, he said.

Andy Cole, chief executive of premature baby charity Bliss, said: “This is a very interesting piece of new research and we always welcome anything that has the potential to improve outcomes for babies born premature or sick.

“This is a cost-effective treatment and could reduce admissions to intensive care services, which are already working at high capacity levels.

“While the early results of this research show benefits to babies born with low blood sugars, it is clear there is more research to be done to implement this treatment.”

Source: BBC

Glucose Levels Predict Risk for Dementia.

Higher glucose levels within the nondiabetic range predicted higher risk for dementia.
Observational studies have established an association between diabetes and dementia. In this prospective study from Seattle’s Group Health Cooperative, researchers sought to determine whether average glucose levels in people without diabetes predict development of dementia. The study involved 2067 older adults (mean age 74; 11% with diabetes) who had no evidence of dementia at baseline and who were screened every 2 years using the Cognitive Abilities Screening Instrument. Average glucose levels were estimated using models that incorporated both serial glycosylated hemoglobin and blood glucose values.

During a median follow-up of 7 years, 25% of participants were diagnosed with dementia. Among participants who did not have diabetes, risk for developing dementia increased with increasing average glucose levels, after adjustment for potentially confounding variables. For example, in those whose average glucose level was 115 mg/dL, relative risk for dementia was 18% higher than in those whose average glucose level was 100 mg/dL. Among participants who had diabetes, relative risk for dementia was 40% higher in those whose average glucose level was 190 mg/dL compared with 160 mg/dL.


The prospective nature of this study, in which patients screened negative for dementia at baseline, is a strength. However, unmeasured confounders might have influenced the association between glycemia and dementia, and reverse causality is remotely possible (e.g., lifestyle changes in patients with early subclinical dementia might promote higher glucose levels). If higher blood glucose levels within the nondiabetic range do contribute to development of dementia, the mechanism is unclear.

Source: NEJM

Elevated Glucose Levels Associated with Dementia.

Higher glucose levels are associated with increased dementia risk, according to a prospective cohort study in the New England Journal of Medicine.

Researchers followed roughly 2100 people aged 65 and older who were free of dementia at baseline. Over a median follow-up of 6.8 years, patients had at least five measurements of glucose or glycated hemoglobin taken. About a quarter of patients developed dementia.

For all participants, the risk for dementia increased with increasing glucose readings. For patients without diabetes, an average glucose level of 115 mg/dL was associated with an 18% higher risk for dementia, compared with a level of 100 mg/dL. For those with diabetes, 190 mg/dL was associated with a 40% increased risk, relative to 160 mg/dL.

The authors speculate that microvascular disease of the central nervous system could contribute to the association.

Source: NEJM