As promised, here is part two of the blog on Agave. I think this will answer a few more questions for you!
Two last points..A recent study in the journal Environmental Health (5), found mercury in nearly 50 percent of the tested samples of commercial high fructose corn syrup (HFCS). A separate study by the Institute for Agriculture and Trade Policy (IATP) detected mercury in nearly one-third of 55 popular brandname food and beverage products where HFCS is the first or second highest labeled ingredient. As the authors concluded, "With respect to total mercury exposure, it may be necessary to account for this source of mercury in the diet of children and sensitive populations." This concern would only relate to HFCS and not Agave.A recent study (6) measured the antioxidant acuity level of several sweeteners and found that refined sugar, corn syrup, and agave nectar contained minimal antioxidant activity, raw cane sugar was slightly higher, and dark and blackstrap molasses had the highest antioxidant activity. Maple syrup, brown sugar, and honey showed intermediate antioxidant capacity.So, lets put all of this in perspective...Are higher levels of fructose in a concentrated caloric sweetener good or bad?Well, if you think HFCS is bad because of the amount of fructose in it, then Agave must be much worse then HFCS.If you think Agave syrup is good because it has a very low GI/GL, as a result of the fructose in it, than HFCS must not be that bad and at least better than table sugar because it has a higher level of fructose in it, and so would have a lower GI/GL than table sugar. So again, are higher levels of fructose in a concentrated caloric sweetener good or bad?We just can't argue it both ways.Now, as we see from these recent studies (1,2), fructose, in excess can create problems as it goes directly to the liver. However, these problems only existed when excess was consumed as there were no negative effects when less than 50 grams was consumed, even when it was pure fructose. So again, the real issue is quantity. If it takes a minimum of 50 grams of fructose to see any negative effect and at least 100 grams of fructose to see a significant negative effect, lets see how these numbers related to potential intakes.To ingest 50 grams fructose, this would be the equivalent of consuming either 100 grams of sucrose, as sucrose is 50/50 glucose/fructose and about 91 grams of HFCS, as HFCS is 55/45 fructose/glucose.To ingest 100 grams of fructose, this would be the equivalent of either 200 grams of sucrose, as sucrose is 50/50 glucose/fructose and about 182 grams of HFCS, as HFCS is 55/45 fructose/glucose.91 grams of HFCS is 370 calories100 grams of sucrose is 400 calories182 grams of HFCS is 740 calories200 grams of Sucrose is 800 caloriesI think anyone would agree that 370 to 400 calories, or 740 to 800 calories of either one as part of daily diet would be considered excess. On a 2000 calorie diet, this would be 19% (at 370 calories) to 40% (at 800 calories) of someone's caloric intake. So, the real issue again, is not which one, but the total amount. The bottom line, no matter which one you choose to use, quantity is the real issue.The recommendation I give in my Label Reading talk is to limit their consumption of all concentrated caloric sweeteners to no more than 5% of calories which for someone consuming 2000 calories is 100 calories per day which is 25 grams or about 2 tablespoons. The only exception I give is that if someone has elevated TGs, or at risk for CVD, then they may want to avoid those higher in fructose. Therefore, limit your consumption of all refined and/or concentrated sweeteners and if heart disease, elevated triglycerides, insulin resistance, diabetes and/or weight are concerns of yours, avoid the ones higher in fructose especially Agave.1) Br J Nutr. 2008 Nov;100(5):947- 52. Consumption of fructose-sweetened beverages for 10 weeks increases postprandial triacylglycerol and apolipoprotein- B concentrations in overweight and obese women. Fructose consumption in the USA has increased over the past three decades. During this time, obesity, insulin resistance and the metabolic syndrome have also increased in prevalence. While diets high in fructose have been shown to promote insulin resistance and increase TAG concentrations in animals, there are insufficient data available regarding the long-term metabolic effects of fructose consumption in humans. The objective of the present study was to investigate the metabolic effects of 10-week consumption of fructose-sweetened beverages in human subjects under energy-balanced conditions in a controlled research setting. Following a 4-week weight-maintaining complex carbohydrate diet, seven overweight or obese (BMI 26.8-33.3 kg/m2) postmenopausal women were fed an isoenergetic intervention diet, which included a fructose-sweetened beverage with each meal, for 10 weeks. The intervention diet provided 15% of energy from protein, 30% from fat and 55% from carbohydrate (30% complex carbohydrate, 25% fructose). Fasting and postprandial glucose, insulin, TAG and apoB concentrations were measured. Fructose consumption increased fasting glucose concentrations and decreased meal-associated glucose and insulin responses (P = 0.0002, P = 0.007 and P = 0.013, respectively). Moreover, after 10 weeks of fructose consumption, 14 h postprandial TAG profiles were significantly increased, with the area under the curve at 10 weeks being 141% higher than at baseline (P = 0.04). Fructose also increased fasting apoB concentrations by 19% (P = 0.043 v. baseline). In summary, consumption of fructose-sweetened beverages increased postprandial TAG and fasting apoB concentrations, and the present results suggest that long-term consumption of diets high in fructose could lead to an increased risk of CVD. PMID: 18384705 2) Am J Clin Nutr. 2008 Nov;88(5):1419- 37. Fructose consumption and consequences for glycation, plasma triacylglycerol, and body weight: meta-analyses and meta-regression models of intervention studies. BACKGROUND: The glycemic response to dietary fructose is low, which may improve concentrations of glycated hemoglobin (HbA(1c), a marker of dysglycemia). Meanwhile, adverse effects on plasma triacylglycerol (a marker of dyslipidemia) and body weight have been questioned. Such effects are reported inconsistently. OBJECTIVE: We aimed to evaluate the effect of fructose on these health markers, particularly examining treatment dose and duration, and level of glycemic control. DESIGN: A literature search was conducted for relevant randomized and controlled intervention studies of crystalline or pure fructose (excluding high-fructose corn syrup), data extraction, meta-analyses, and modeling using meta-regression. RESULTS: Fructose intake < 90 g/d significantly improved HbA(1c) concentrations dependent on the dose, the duration of study, and the continuous severity of dysglycemia throughout the range of dysglycemia. There was no significant change in body weight at intakes <100 g fructose/d. Fructose intakes of <50 g/d had no postprandially significant effect on triacylglycerol and those of