mayku-T-meelo
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Can you please link it? I can't find it by searching with keywords.
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Sucrose is the primary source of modern disease
- Thread starter Alpha
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Can you please link it? I can't find it by searching with keywords.
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Hi Mauritio, Aldolase B and Fructokinase Isoform C are mainly present in the liver, and to some degree the intestines as well. The main role of the intestine is to break down sucrose using sucrase into glucose and fructose for transport through the epithelium primarily through GLUT5. This is a good study you posted, one that I haven't seen before, although done in mice, I will try to look for replicated findings done in humans.
These results suggest that sucrose and free fructose are metabolically equivalent and are consistent with literature indicating that consumption of sugar and of high-fructose corn syrup has similar pathological effects (Tappy and Le, 2010).
However, it was shown that liver fructose and its metabolites increase in the liver in a dose-dependent manner
That was mostly achieved through the upregulation of GLUT5.
These measures may sometimes be misleading because FK or KHK as it's otherwise known can alternatively lead to high Fructose 1-Phosphate which will not show up in portal vein concentration assays. This needs to be further studies in humans using carbon isotopes tracking fructose down the intestinal tract, if you happen to find one let me know. I don't deny that some of the fructose that isn't rapidly absorbed in the upper lining of the small intestines when it makes its way down toward the ileum and colon can negatively affect gut microbiota and aggravating the issue. I've already posted studies where TLR4 KO or antibiotics do ameliorate NAFLD and steatosis to a large degree, but it does not completely prevent it, and likely only slowly progresses it, if you have a study for a long enough period.
There are few estimates of portal fructose concentrations (102). This is unfortunate because NAFLD, now estimated to affect almost one billion individuals worldwide, has been associated with high intakes of dietary fructose (120), increasing concentrations in the portal vein. Intestinal absorption seems to be the primary regulator of portal fructose concentrations, which increase only in animals actively consuming high-fructose diets. In rats fed a bolus of 2-g/kg sucrose (equivalent to about three cans of regular soda in humans), portal fructose concentrations increased rapidly from ∼0.1 to 1 mM (124). In baboons gavaged with 2-g/kg sucrose, fructose levels in the portal blood increased to 1.9 mM (12). Compared to those fed 20% glucose, wild-type mice fed an isocaloric diet containing 20% fructose maintained a 2.5-fold higher (∼0.13 mM) portal fructose concentration (102). Portal fructose levels drop within hours when wild-type mice cease feeding. In actively feeding, global KHK−/− mice, portal fructose concentrations were already high (∼0.8 mM) with the 20% glucose diet, then increased twofold with the 20% fructose diet. Since portal fructose levels are fivefold lower in wild-type mice fed the same 20% fructose diet, intestinal KHK in wild-type mice may catabolize fructose in enterocytes prior to release in portal circulation, lowering portal fructose levels. - Ronaldo P. Ferraris, Jun-yong Choe, Chirag R. Patel. Annual Review of Nutrition 2018 38:1, 41-67
Mechanisms Of Fructose Absorption : Clinical and Translational Gastroenterology
An abstract is unavailable.
journals.lww.com
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Farkhondeh Alami, Mohammad Alizadeh & Kamran Shateri (2022) The effect of a fruit-rich diet on liver biomarkers, insulin resistance, and lipid profile in patients with non-alcoholic fatty liver disease: a randomized clinical trial, Scandinavian Journal of Gastroenterology, 57:10, 1238-1249, DOI: 10.1080/00365521.2022.2071109
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Hi revenant, I discuss extensively in this thread why Longitudinal studies are critical in studying changing biomarkers with different diet patterns, while this study was done with 2 overfeeding sessions. Nevertheless, there were some issues with the study, mainly the high fat intake that was only 20% less than carbohydrates, and the undetailed form of dietary fat consumed. The literature is clear that in excess energy consumption accompanying high fat intake, the body will preferentially store the fatty acids from the diet while oxidizing the protein or carbohydrates consumed for a more efficient resource allocation. The study would have been better done isocalorically using very low-fat diets instead, and over long periods. Despite that, you can clearly see the average fat deposits estimated (crudely at that) was 15% higher on average in the sucrose group compared to the glucose group.
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Hi ATP, I've already gave some studies showing the impact of sucrose or fructose in multiple experimental designs.
Here's some findings from meta-analysis studies on the effects of sucrose or fructose in Humans.
The Nurses study is partciularly a great one, and constantly cited by the AHA in their conferences. it showed a 1.22 Hazard ratio for sucrose consumption and CVD incidence.
The authors looked at an estimated linear and spline model to predict the dose-dependency on the outcomes. The outer lines are the confidence intervals.
Here is another meta analysis showing CVD mortatlty
Another RCT done in Denmark using either regular cola, semi-skimmed milk, diet cola, or water isocalorically measured intrahepatic fat and intramyocellular fat.
The relative changes between baseline and the end of 6-mo intervention were significantly higher in the regular cola group than in the 3 other groups for liver fat (132-143%, sex-adjusted mean; P < 0.01), skeletal muscle fat (117-221%; P < 0.05), visceral fat (24-31%; P < 0.05), blood triglycerides (32%; P < 0.01), and total cholesterol (11%; P < 0.01). Total fat mass was not significantly different between the 4 beverage groups. Milk and diet cola reduced systolic blood pressure by 10-15% compared with regular cola (P < 0.05). Otherwise, diet cola had effects similar to those of water. - Maersk, Maria et al.
Sucrose-sweetened beverages increase fat storage in the liver, muscle, and visceral fat depot: a 6-mo randomized intervention study - PubMed
Daily intake of SSSDs for 6 mo increases ectopic fat accumulation and lipids compared with milk, diet cola, and water. Thus, daily intake of SSSDs is likely to enhance the risk of cardiovascular and metabolic diseases. This trial is registered at clinicaltrials.gov as NCT00777647.
pubmed.ncbi.nlm.nih.gov
Fructose showed statisticalally significant increase in BW and partcularly in Abdominal and visceral adipose tissue.
Fructose more reliably and more strongly increased cirtculating triglycerides, an important marker of DNL and CVD.
APOB was higher with statistical significance in fructose vs glucose, the gold standard for measuring CVD risk.
DNL fractionation assays showed higher lipogenesis from Fructose compared to just glucose.
Insulin resistance and insulin response was worse with Fructose compared to Glucose, despite Fructose being insulin independent.
The authors propse the mechanism for why the difference exists, this has been discussed before extensively in this thread to name a few.
We reached the following conclusions: (a) The increase in VAT in subjects consuming fructose and the increase in the expression of lipogenic genes in SAT in subjects consuming glucose suggest that fructose and glucose have differential effects on regional adipose distribution. We believe that these results are novel and warrant further investigation. (b) In addition to increases of postprandial TG and fasting and postprandial apoB, we show for what we believe is the first time that fructose consumption increases plasma concentrations of fasting sdLDL, oxidized LDL, and postprandial RLP-C and RLP-TG in older, overweight/obese men and women, whereas glucose consumption does not. These changes may be associated with an increased risk of cardiovascular disease (30, 36, 45, 64–66). (c) Fructose consumption increased hepatic fractional DNL, and postprandial LPL activity was lower in subjects consuming fructose compared with those consuming glucose. These results suggest that both increased DNL and decreased LPL-mediated clearance contribute to fructose-induced postprandial hypertriglyceridemia. (d) Consumption of fructose at 25% of energy requirements with an ad libitum diet decreased glucose tolerance and insulin sensitivity in older overweight/obese adults compared with glucose consumption. (e) VAT accumulation and increases of 24-hour TG exposure, peak postprandial TG concentrations, and postprandial RLP-C concentrations in response to fructose consumption were more pronounced in men than in women. Consumption of sugar-sweetened beverages resulted in greater decreases in insulin sensitivity in women than in men. - J Clin Invest. 2009;119(5):1322-1334. JCI - Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans.
Here is a randomized control trial using sucrose(the topic of this thread) with human subjects that didn’t use ridiculous overfeeding or an unrealistic diet. RCTs are considered the highest level of evidence available.
diabetesjournals.org
“In this study, a high-sucrose intake as part of an eucaloric, weight-maintaining diet had no detrimental effect on insulin sensitivity, glycemic profiles, or measures of vascular compliance in healthy nondiabetic subjects.”
“Evidence from animal studies has generally shown that increased sucrose intake has a detrimental effect on insulin sensitivity and cardiovascular risk factors. However, the levels of sucrose intake in these studies, of up to 60–70% of dietary energy intake as sucrose or fructose, have generally been at a level that is nonphysiological and, for most human subjects, unpalatable. Furthermore, the diets studied were in many cases hypercaloric, making interpretation of the relative impact of sucrose intake and weight gain impossible”
“We found no difference in peripheral insulin resistance between the two dietary periods. The study was powered to exclude a 10% difference in insulin action, which is a level assumed likely to have a clinically relevant impact. The results in fact showed a trend toward an increase in insulin sensitivity with the high-sucrose diet, although this was not statistically significant.”
“Furthermore, we found no difference in fasting levels of serum nonesterified fatty acid concentrations during the dietary periods and a comparable degree of suppression during hyperinsulinemia, indicating no detrimental effect on adipose tissue insulin action.”
“In this study, continuous monitoring of interstitial glucose levels using a continuous glucose monitoring system showed no difference in 24-h or postprandial glycemic exposure.”
“caloric intakes were controlled rather than ad libitum to allow conclusions to be drawn regarding carbohydrate quality itself rather than the complicating factor of differing energy intakes and balances.”
“In conclusion, a high-sucrose intake as part of a balanced, eucaloric, weight-maintaining diet had no detrimental effect on insulin sensitivity in healthy nondiabetic subjects compared with a low-sucrose diet. These results suggest that important pathogenic processes that precede diabetes and vascular disease are not significantly worsened by sucrose itself. ”
Effect of Eucaloric High- and Low-Sucrose Diets With Identical Macronutrient Profile on Insulin Resistance and Vascular Risk: A Randomized Controlled Trial
The long-term impact of dietary carbohydrate type, in particular sucrose, on insulin resistance and the development of diabetes and atherosclerosis is not
diabetesjournals.org
“In this study, a high-sucrose intake as part of an eucaloric, weight-maintaining diet had no detrimental effect on insulin sensitivity, glycemic profiles, or measures of vascular compliance in healthy nondiabetic subjects.”
“Evidence from animal studies has generally shown that increased sucrose intake has a detrimental effect on insulin sensitivity and cardiovascular risk factors. However, the levels of sucrose intake in these studies, of up to 60–70% of dietary energy intake as sucrose or fructose, have generally been at a level that is nonphysiological and, for most human subjects, unpalatable. Furthermore, the diets studied were in many cases hypercaloric, making interpretation of the relative impact of sucrose intake and weight gain impossible”
“We found no difference in peripheral insulin resistance between the two dietary periods. The study was powered to exclude a 10% difference in insulin action, which is a level assumed likely to have a clinically relevant impact. The results in fact showed a trend toward an increase in insulin sensitivity with the high-sucrose diet, although this was not statistically significant.”
“Furthermore, we found no difference in fasting levels of serum nonesterified fatty acid concentrations during the dietary periods and a comparable degree of suppression during hyperinsulinemia, indicating no detrimental effect on adipose tissue insulin action.”
“In this study, continuous monitoring of interstitial glucose levels using a continuous glucose monitoring system showed no difference in 24-h or postprandial glycemic exposure.”
“caloric intakes were controlled rather than ad libitum to allow conclusions to be drawn regarding carbohydrate quality itself rather than the complicating factor of differing energy intakes and balances.”
“In conclusion, a high-sucrose intake as part of a balanced, eucaloric, weight-maintaining diet had no detrimental effect on insulin sensitivity in healthy nondiabetic subjects compared with a low-sucrose diet. These results suggest that important pathogenic processes that precede diabetes and vascular disease are not significantly worsened by sucrose itself. ”
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Another study in obese subjects using sucrose/hfcs as part of a eucaloric diet.
www.ncbi.nlm.nih.gov
“Sixty five overweight and obese individuals were placed on a eucaloric (weight stable) diet for 10-weeks, which incorporated sucrose- or HFCS-sweetened, low-fat milk at 10% or 20% of calories in a randomized, double-blinded study. All groups responded similarly (interaction p > 0.05). There was no change in body weight in any of the groups over the 10-week study, or in systolic or diastolic blood pressure. Likewise, there were no changes in total cholesterol, triglycerides, low-density lipoprotein (LDL), or apolipoprotein B (Apo B). We conclude that (1) when consumed as part of a eucaloric diet fructose—when given with glucose (as normally consumed) does not promote weight gain or an atherogenic lipid profile even when consumed at two to four times the level recently recommended by the AHA. (2) There were no differences between HFCS and sucrose on these parameters.”
“Our main findings are: (1) when consumed as part of a eucaloric (weight-stable) diet for a 10-week period, fructose containing sugars do not promote weight gain or an atherogenic lipid profile even when consumed at two to four times the level currently recommended by the AHA [9]; and (2) there are no differences between sucrose and HFCS in these measures at typical levels of sweetener consumption.”
The Effect of Normally Consumed Amounts of Sucrose or High Fructose Corn Syrup on Lipid Profiles, Body Composition and Related Parameters in Overweight/Obese Subjects
The American Heart Association (AHA) has advocated that women and men not consume more than 100 and 150 kcal/day, respectively, from added sugars. These levels are currently exceeded by over 90% of the adult population in the United States. Few data exist ...
www.ncbi.nlm.nih.gov
“Sixty five overweight and obese individuals were placed on a eucaloric (weight stable) diet for 10-weeks, which incorporated sucrose- or HFCS-sweetened, low-fat milk at 10% or 20% of calories in a randomized, double-blinded study. All groups responded similarly (interaction p > 0.05). There was no change in body weight in any of the groups over the 10-week study, or in systolic or diastolic blood pressure. Likewise, there were no changes in total cholesterol, triglycerides, low-density lipoprotein (LDL), or apolipoprotein B (Apo B). We conclude that (1) when consumed as part of a eucaloric diet fructose—when given with glucose (as normally consumed) does not promote weight gain or an atherogenic lipid profile even when consumed at two to four times the level recently recommended by the AHA. (2) There were no differences between HFCS and sucrose on these parameters.”
“Our main findings are: (1) when consumed as part of a eucaloric (weight-stable) diet for a 10-week period, fructose containing sugars do not promote weight gain or an atherogenic lipid profile even when consumed at two to four times the level currently recommended by the AHA [9]; and (2) there are no differences between sucrose and HFCS in these measures at typical levels of sweetener consumption.”
Systematic Review
Abstract: “We systematically reviewed interventions substituting sucrose for other macronutrients in apparently healthy adults to assess impact on cardiometabolic risk indicators. Multiple databases were searched to January 2012 and abstracts assessed by 2 reviewers. Twenty-five studies (29 papers) met inclusion criteria but varied in quality and duration. Weaknesses included small subject numbers, unclear reporting of allocation, unusual dietary regimes, differences in energy intake, fat composition or fibre between conditions, unhealthy subjects, heterogeneity of results, and selective reporting. Insufficient data were available to draw reliable conclusions except with regard to the substitution of sucrose for starch, where effects on plasma lipids were inconsistent, mostly explicable by other factors, or nonsignificant. Based on fewer studies, there was little evidence for significant effects on plasma glucose or insulin. Sucrose substitution for starch up to 25% energy does not appear to have adverse effects on cardiometabolic risk indicators in apparently healthy adults. Furthermore, there is no consistent evidence that restricting sucrose in an isoenergetic diet would affect risk indicators, except perhaps in people with certain preexisting metabolic abnormalities.”
www.ncbi.nlm.nih.gov
“The above studies fed under controlled isocaloric conditions fail to demonstrate a consistent or meaningful adverse effect of sucrose at a level up to 25% energy in healthy young adults, although this cannot be extrapolated to adults with dyslipidemia or diabetes. ”
“In a study comparing sucrose with fructose, Bosetti et al., compared isocaloric diets at a realistic level of consumption (15% energy) using typical American foods for 14 days in a crossover study. There was no change in total TG, TC, LDL cholesterol, or HDL cholesterol concentrations between diet periods. They concluded that there is no difference between sucrose or fructose on various lipid components in the “real world” in normal subjects (Bossetti et al., 1984). Similarly, in a crossover study using fructose, sucrose, and glucose drinks for 3 weeks, lipoprotein concentrations were unchanged on all conditions, and sucrose and fructose results were similar with regard to LDL subclass distribution (Aeberli et al., 2011).”
“One metabolic ward study in healthy young men aged 18–22 years found that a supra-physiologic level of sucrose over a relatively short time period resulted in an improvement of glucose tolerance. Increasing sucrose content to 40% for 4–5 days improved both oral and intravenous glucose tolerance compared with a control/normal diet (17:43:40 protein:fat:CHO; Anderson et al., 1973). Glucose tolerance continued to improve with the 80% sucrose diet administered for up to 65 days, an effect accompanied by a reduction in fasting plasma insulin. ”
Abstract: “We systematically reviewed interventions substituting sucrose for other macronutrients in apparently healthy adults to assess impact on cardiometabolic risk indicators. Multiple databases were searched to January 2012 and abstracts assessed by 2 reviewers. Twenty-five studies (29 papers) met inclusion criteria but varied in quality and duration. Weaknesses included small subject numbers, unclear reporting of allocation, unusual dietary regimes, differences in energy intake, fat composition or fibre between conditions, unhealthy subjects, heterogeneity of results, and selective reporting. Insufficient data were available to draw reliable conclusions except with regard to the substitution of sucrose for starch, where effects on plasma lipids were inconsistent, mostly explicable by other factors, or nonsignificant. Based on fewer studies, there was little evidence for significant effects on plasma glucose or insulin. Sucrose substitution for starch up to 25% energy does not appear to have adverse effects on cardiometabolic risk indicators in apparently healthy adults. Furthermore, there is no consistent evidence that restricting sucrose in an isoenergetic diet would affect risk indicators, except perhaps in people with certain preexisting metabolic abnormalities.”
The Effects of Sucrose on Metabolic Health: A Systematic Review of Human Intervention Studies in Healthy Adults
We systematically reviewed interventions substituting sucrose for other macronutrients in apparently healthy adults to assess impact on cardiometabolic risk indicators. Multiple databases were searched to January 2012 and abstracts assessed by 2 reviewers. ...
www.ncbi.nlm.nih.gov
“The above studies fed under controlled isocaloric conditions fail to demonstrate a consistent or meaningful adverse effect of sucrose at a level up to 25% energy in healthy young adults, although this cannot be extrapolated to adults with dyslipidemia or diabetes. ”
“In a study comparing sucrose with fructose, Bosetti et al., compared isocaloric diets at a realistic level of consumption (15% energy) using typical American foods for 14 days in a crossover study. There was no change in total TG, TC, LDL cholesterol, or HDL cholesterol concentrations between diet periods. They concluded that there is no difference between sucrose or fructose on various lipid components in the “real world” in normal subjects (Bossetti et al., 1984). Similarly, in a crossover study using fructose, sucrose, and glucose drinks for 3 weeks, lipoprotein concentrations were unchanged on all conditions, and sucrose and fructose results were similar with regard to LDL subclass distribution (Aeberli et al., 2011).”
“One metabolic ward study in healthy young men aged 18–22 years found that a supra-physiologic level of sucrose over a relatively short time period resulted in an improvement of glucose tolerance. Increasing sucrose content to 40% for 4–5 days improved both oral and intravenous glucose tolerance compared with a control/normal diet (17:43:40 protein:fat:CHO; Anderson et al., 1973). Glucose tolerance continued to improve with the 80% sucrose diet administered for up to 65 days, an effect accompanied by a reduction in fasting plasma insulin. ”
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Systematic Review
Abstract: “We systematically reviewed interventions substituting sucrose for other macronutrients in apparently healthy adults to assess impact on cardiometabolic risk indicators. Multiple databases were searched to January 2012 and abstracts assessed by 2 reviewers. Twenty-five studies (29 papers) met inclusion criteria but varied in quality and duration. Weaknesses included small subject numbers, unclear reporting of allocation, unusual dietary regimes, differences in energy intake, fat composition or fibre between conditions, unhealthy subjects, heterogeneity of results, and selective reporting. Insufficient data were available to draw reliable conclusions except with regard to the substitution of sucrose for starch, where effects on plasma lipids were inconsistent, mostly explicable by other factors, or nonsignificant. Based on fewer studies, there was little evidence for significant effects on plasma glucose or insulin. Sucrose substitution for starch up to 25% energy does not appear to have adverse effects on cardiometabolic risk indicators in apparently healthy adults. Furthermore, there is no consistent evidence that restricting sucrose in an isoenergetic diet would affect risk indicators, except perhaps in people with certain preexisting metabolic abnormalities.”
The Effects of Sucrose on Metabolic Health: A Systematic Review of Human Intervention Studies in Healthy Adults
We systematically reviewed interventions substituting sucrose for other macronutrients in apparently healthy adults to assess impact on cardiometabolic risk indicators. Multiple databases were searched to January 2012 and abstracts assessed by 2 reviewers. ...
“The above studies fed under controlled isocaloric conditions fail to demonstrate a consistent or meaningful adverse effect of sucrose at a level up to 25% energy in healthy young adults, although this cannot be extrapolated to adults with dyslipidemia or diabetes. ”
“In a study comparing sucrose with fructose, Bosetti et al., compared isocaloric diets at a realistic level of consumption (15% energy) using typical American foods for 14 days in a crossover study. There was no change in total TG, TC, LDL cholesterol, or HDL cholesterol concentrations between diet periods. They concluded that there is no difference between sucrose or fructose on various lipid components in the “real world” in normal subjects (Bossetti et al., 1984). Similarly, in a crossover study using fructose, sucrose, and glucose drinks for 3 weeks, lipoprotein concentrations were unchanged on all conditions, and sucrose and fructose results were similar with regard to LDL subclass distribution (Aeberli et al., 2011).”
“One metabolic ward study in healthy young men aged 18–22 years found that a supra-physiologic level of sucrose over a relatively short time period resulted in an improvement of glucose tolerance. Increasing sucrose content to 40% for 4–5 days improved both oral and intravenous glucose tolerance compared with a control/normal diet (17:43:40 protein:fat:CHO; Anderson et al., 1973). Glucose tolerance continued to improve with the 80% sucrose diet administered for up to 65 days, an effect accompanied by a reduction in fasting plasma insulin. ”
Hi Jamsey, thanks for the studies. This is from the table in the meta analysis you posted.
Reference | Sucrose% | Outcomes | Result | Authors conclusion | Comments |
|---|---|---|---|---|---|
19% | TC, LDL, HDL, TG, LDL particle size and distribution, fasting glucose, IR, C-reactive protein, BP | NSD in TC, LDL, HDL, or TG. LDL particle size (LDL1) lower on high sucrose and high fructose but not high glucose. No increase in small dense LDL. NSD in fasting glucose (slight rise compared with baseline). | High sucrose and high fructose beverage conditions showed similar effects on LDL particle size. High glucose condition did not. | More data required on significance of LDL particle size. (Data now show it is very significant) | |
∼15% | TC, TGs, LDL, HDL, LDL:HDL, insulin, glucose, insulin:glucose ratio | NSD on any outcome on either diet at 7 or 14 days. HTG subject had increased TGs on sucrose diet. | Physiological amounts of sucrose have the same effect on metabolic outcomes as fructose. | EI determined by food diary before experiment, so difficult to determine exact%sucrose. | |
16% | TG, TC | In subjects whose weight remained unchanged there was a sig. (8%) fall in TC (p < 0.025) and phospholipid-P (p < 0.025) in the glucose-syrup period but TG did not change. | Changes in some blood lipids may be attributed to the isoenergetic replacement of table sucrose by glucose syrup. | Longest study. Suggests small but sig. beneficial effects on TC of replacing sucrose with glucose. | |
(Fry, 1972) | ∼12.5% | GTT every 3 weeks | Sig. higher blood glucose at 0.5 hr on normal sucrose diet (p < 0.001), but lower at 1 and 1.5 hr (p < 0.05). NSD on AUC (mean of last 3 GTTs on each diet). | There is a change in glucose tolerance when changing from a sucrose-free to sucrose-containing diet. Post-prandial glucose curve may be flatter with glucose than sucrose but NSD in AUC. | Subjects were men in British Antarctic survey |
10–13% | TG, cholesterol, and phospholipids | Overall NSD in TG during low sucrose diet. However 10% fall for high TG group (p < 0.01) (not correlated with body weight changes). NSD for low TG group. TC fell during sucrose-free diet in the high TC group, but rose in the low TC group. NSD in phospholipids. | Sucrose reduced diets may lower TGs in those with high levels at baseline, which seems to be an effect of sucrose restriction rather than weight loss.The effect on cholesterol is less clear. | The sig. reduction in the high TG group should be viewed with caution (Mann et al., 1973) and may be regression to mean (no control group). Does not constitute evidence of a sucrose effect on TG, independent of weight loss. | |
45% and 65% | TG, 24 hr TG (AUC) | Fasting TG increased on 65% CHO diet versus 45% CHO but NSD between sucrose and corn syrup. However 24-hr TG concentration was higher on sucrose diet versus corn syrup (112 vs. 91 mg/dl at 45%; 129 vs. 94 mg/dl at 65%). | High sucrose diet at 45% or 65% energy induces higher 24 hr TG response than corn syrup diet of equivalent composition. |
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Another study in obese subjects using sucrose/hfcs as part of a eucaloric diet.
The Effect of Normally Consumed Amounts of Sucrose or High Fructose Corn Syrup on Lipid Profiles, Body Composition and Related Parameters in Overweight/Obese Subjects
The American Heart Association (AHA) has advocated that women and men not consume more than 100 and 150 kcal/day, respectively, from added sugars. These levels are currently exceeded by over 90% of the adult population in the United States. Few data exist ...
“Sixty five overweight and obese individuals were placed on a eucaloric (weight stable) diet for 10-weeks, which incorporated sucrose- or HFCS-sweetened, low-fat milk at 10% or 20% of calories in a randomized, double-blinded study. All groups responded similarly (interaction p > 0.05). There was no change in body weight in any of the groups over the 10-week study, or in systolic or diastolic blood pressure. Likewise, there were no changes in total cholesterol, triglycerides, low-density lipoprotein (LDL), or apolipoprotein B (Apo B). We conclude that (1) when consumed as part of a eucaloric diet fructose—when given with glucose (as normally consumed) does not promote weight gain or an atherogenic lipid profile even when consumed at two to four times the level recently recommended by the AHA. (2) There were no differences between HFCS and sucrose on these parameters.”
“Our main findings are: (1) when consumed as part of a eucaloric (weight-stable) diet for a 10-week period, fructose containing sugars do not promote weight gain or an atherogenic lipid profile even when consumed at two to four times the level currently recommended by the AHA [9]; and (2) there are no differences between sucrose and HFCS in these measures at typical levels of sweetener consumption.”
The subjects were consuming really high sugar before the study at baseline, I'm not sure if increasing further would add to the detrimental effects. The difference in calorie consumption in sucrose 20% diet is also a little surprising, that looks rather low given that they are the same weight and 67% male vs 30% male in the 10% sucrose group.
Table 3
Changes in macronutrient profile of the diet after ten weeks of sugar sweetened milk consumption as part of a eucaloric diet.Variable | Time | HFCS 10% | HFCS 20% | Suc 10% | Suc 20% | All |
|---|---|---|---|---|---|---|
Energy Intake | Baseline | 2204 ± 1076 | 2115 ± 477 | 2542 ± 1407 | 2086 ± 964 | 2260 ± 1048 |
(kcal) | Week 10 | 2588 ± 758 | 2546 ± 836 | 2970 ± 1786 | 2328 ± 686 | 2644 ± 1160 *** |
| | Interaction p = 0.925 | | | | |
Carbohydrate | Baseline | 273.6 ± 125.1 | 255.9 ± 62.6 | 323.4 ± 178.2 | 236.6 ± 102.3 | 277.2 ± 129.2 |
(g) | Week 10 | 341.6 ± 97.5 | 374.3 ± 132.2 | 383.0 ± 242.2 | 348.6 ± 102.0 | 363.4 ± 158.8 *** |
| | Interaction p = 0.389 | | | | |
Fat | Baseline | 83.5 ± 57.2 | 82.2 ± 26.5 | 94.9 ± 58.5 | 90.8 ± 53.7 | 87.7 ± 49.8 |
(g) | Week 10 | 86.2 ± 38.2 | 72.2 ± 30.7 | 99.4 ± 66.9 | 62.2 ± 23.4 | 82.3 ± 46.4 |
| | Interaction p = 0.074 | | | | |
Protein | Baseline | 89.6 ± 28.2 | 91.8 ± 22.7 | 99.7 ± 59.7 | 85.9 ± 39.2 | 92.5 ± 40.1 |
(g) | Week 10 | 122.0 ± 31.9 | 109.1 ± 33.8 | 144.2 ± 69.5 | 108.0 ± 29.7 | 122.7 ± 47.6 *** |
| | Interaction p = 0.165 | | | | |
Total Sugar | Baseline | 126.4 ± 65.9 | 110.6 ± 43.2 | 154.4 ± 121.0 | 108.9 ± 69.2 | 127.5 ± 82.6 |
(g) | Week 10 | 199.6 ± 56.1 *** | 247.9 ± 99.5 *** | 218.8 ± 144.6 ** | 215.4 ± 83.6 *** | 220.5 ± 102.7 *** |
| | Interaction p < 0.05 | | | |
Changes in body mass, body composition and waist circumference after ten weeks of sugar sweetened milk consumption as part of a eucaloric diet.
Variable | Time | HFCS 10% | HFCS 20% | Suc 10% | Suc 20% | All |
|---|---|---|---|---|---|---|
Body Mass | Baseline | 185.4 ± 44.3 | 184.5 ± 35.3 | 179.3 ± 34.4 | 182.2 ± 39.9 | 182.8 ± 37.7 |
(lbs) | Week 10 | 186.2 ± 43.9 | 187.9 ± 36.0 | 181.4 ± 33.9 | 184.4 ± 41.1 | 185.0 ± 37.9 ** |
| | Interaction p = 0.507 | | | | |
Waist | Baseline | 90.4 ± 13.5 | 90.9 ± 14.0 | 88.6 ± 11.2 | 90.2 ± 11.6 | 90.0 ± 12.4 |
(cm) | Week10 | 90.2 ± 13.2 | 91.8 ± 14.2 | 89.5 ± 11.1 | 90.6 ± 12.1 | 90.5 ± 12.4 |
| | Interaction p = 0.678 | | | | |
Body Fat | Baseline | 35.6 ± 7.3 | 38.7 ± 7.2 | 32.6 ± 9.2 | 37.7 ± 4.8 | 36.0 ± 7.7 |
(%) | Week 10 | 35.8 ± 7.3 | 38.8 ± 7.0 | 33.8 ± 9.1 | 38.1 ± 5.0 | 36.5 ± 7.5 ** |
| | Interaction p = 0.075 | | | | |
Fat Mass | Baseline | 64.2 ±23.5 | 68.0 ± 15.5 | 57.3 ± 23.0 | 66.4 ± 16.2 | 63.7 ± 20.1 |
(lbs) | Week 10 | 64.8 ± 23.0 | 69.5 ± 15.9 | 59.7 ± 22.6 | 68.2 ± 17.7 | 65.3 ± 20.1 ** |
| | Interaction p = 0.532 | | | | |
Fat Free Mass | Baseline | 120.3 ± 27.0 | 115.3 ± 28.5 | 121.7 ± 21.7 | 114.3 ± 26.3 | 118.1 ± 26.0 |
(lbs) | Week 10 | 120.9 ± 29.3 | 116.9 = 28.1 | 120.8 ± 22.0 | 117.3 ± 27.9 | 118.6 ± 26.3 |
| | Interaction p = 0.080 | | |
The starting weights also didn't add up, so I redid them using the sum of lean mass and fat mass, Sucrose 20% group gained 2.7% weight over a 10-week period, despite consuming 20% less calories in the 10% sucrose group.
In the current study, there was an overall decrease in HDL (p < 0.01) and increase in total cholesterol to HDL ratio (p < 0.01), however these measures were unaffected by treatment group (interaction p > 0.05). In the current study, there was an overall decrease in HDL (p < 0.01) and increase in total cholesterol to HDL ratio (p < 0.01), however these measures were unaffected by treatment group (interaction p > 0.05). The observed response in triglycerides in HFCS 20% was not a surprising observation. Increased intake of carbohydrates has been shown to promote formation of nascent very-low-density lipoprotein (VLDL) particles by combining glycerol, free fatty acids and Apo B, thus increasing plasma triglycerides Although our study was not designed the explore the hepatic synthesis of VLDL the increased Apo B observed in this group supports our speculation. It should also be noted that the sugars were delivered in 1% milk and as a result total protein intake also increased. This may have altered the food intake and also hepatic lipid metabolism. Thus, our reported results, related to lipid parameters must be treated with some caution.
Weaknesses of the current study include that subjects were only followed for 10 weeks and that children, adolescents and individuals over the age of 60 were excluded. Further studies employing larger numbers of subjects, different population groups (e.g., adolescents and individuals over the age of 60) may be warranted.
Yeah, if you actually read the study, you would have found that they also reviewed those findings and concluded this
“Thus, while these studies provide some evidence for an increase in plasma lipids, especially TG in men over the short term (1–2 weeks), the effect is modest and not consistent across studies. Furthermore, intake in these protocols is at least 3 times the mean estimated intake of normal adults.”
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People tend to dump studies or read abstracts without actually reading it in full. This will probably be the last study I dive deep into from another user, if you aren't willing to read it fully yourself, don't bother posting it.Here is a randomized control trial using sucrose(the topic of this thread) with human subjects that didn’t use ridiculous overfeeding or an unrealistic diet. RCTs are considered the highest level of evidence available.
Effect of Eucaloric High- and Low-Sucrose Diets With Identical Macronutrient Profile on Insulin Resistance and Vascular Risk: A Randomized Controlled Trial
The long-term impact of dietary carbohydrate type, in particular sucrose, on insulin resistance and the development of diabetes and atherosclerosis is not
“In this study, a high-sucrose intake as part of an eucaloric, weight-maintaining diet had no detrimental effect on insulin sensitivity, glycemic profiles, or measures of vascular compliance in healthy nondiabetic subjects.”
“Evidence from animal studies has generally shown that increased sucrose intake has a detrimental effect on insulin sensitivity and cardiovascular risk factors. However, the levels of sucrose intake in these studies, of up to 60–70% of dietary energy intake as sucrose or fructose, have generally been at a level that is nonphysiological and, for most human subjects, unpalatable. Furthermore, the diets studied were in many cases hypercaloric, making interpretation of the relative impact of sucrose intake and weight gain impossible”
“We found no difference in peripheral insulin resistance between the two dietary periods. The study was powered to exclude a 10% difference in insulin action, which is a level assumed likely to have a clinically relevant impact. The results in fact showed a trend toward an increase in insulin sensitivity with the high-sucrose diet, although this was not statistically significant.”
“Furthermore, we found no difference in fasting levels of serum nonesterified fatty acid concentrations during the dietary periods and a comparable degree of suppression during hyperinsulinemia, indicating no detrimental effect on adipose tissue insulin action.”
“In this study, continuous monitoring of interstitial glucose levels using a continuous glucose monitoring system showed no difference in 24-h or postprandial glycemic exposure.”
“caloric intakes were controlled rather than ad libitum to allow conclusions to be drawn regarding carbohydrate quality itself rather than the complicating factor of differing energy intakes and balances.”
“In conclusion, a high-sucrose intake as part of a balanced, eucaloric, weight-maintaining diet had no detrimental effect on insulin sensitivity in healthy nondiabetic subjects compared with a low-sucrose diet. These results suggest that important pathogenic processes that precede diabetes and vascular disease are not significantly worsened by sucrose itself. ”
First, the study is significantly underpowered, it's using only 13 subjects, and I keep mention the important of proper longitudinal studies, while the intervention period here was only for 6 weeks.
The diets were generally quite healthy, really high in vegetables and moderatly high in fruits representing the sugars. Total calories were 3,200/day, implying 80g of sugar for the first group and 200g for the second group.
| Meal | 10% sucrose diet (13.3 mJ) | 25% sucrose diet (13.4 mJ) |
|---|---|---|
| Breakfast | Cornflakes (60 g) | Cornflakes (35 g), bran-based cereal (3 g) |
| Semiskimmed milk (167 g) | Semiskimmed milk (160 g) | |
| Sugar (10 g) | Sugar (15 g) | |
| White bread, toasted (31 g) | Pineapple juice (200 g) | |
| Strawberry jam (20 g) | ||
| Orange juice (200 g) |
| Lunch | White bread (150 g) | Wholemeal bread (72 g) |
| Cooked ham (70 g) | Cooked ham (69 g) | |
| Mayonnaise (40 g) | Mayonnaise (32 g) | |
| Yogurt with fruit purée (175 g) | Yogurt with fruit purée (175 g) | |
| Carbonated orange drink (330 g) |
| Dinner | Potatoes, boiled (450 g) | Potatoes, boiled (400 g) |
| Broccoli, boiled (85 g) | Broccoli, boiled (85 g) | |
| Carrots, boiled (80 g) | Carrots, boiled (80 g) | |
| Chicken breast in crumbs, baked (90 g) | Chicken breast in crumbs, baked (90 g) | |
| Gravy, reconstituted (160 g) | Gravy, reconstituted (70 g) | |
| Carbonated orange drink (330 g) |
| Additional snacks | Semiskimmed milk (80 g) | Semiskimmed milk (80 g) |
| Chocolate biscuit bar (48 g) | Smartie-type sweets (80 g) | |
| Chocolate candy bar (52 g) | Chocolate nut bar (60 g) | |
| Plain potato chips (55 g) | Vanilla fudge (40 g) | |
| White bread, toasted (72 g) | Milk chocolate (68 g) | |
| Polyunsaturated margarine (15 g) | Apple (170 g) | |
| Polyunsaturated margarine (15 g) |
Using Google, sugar content distribution was approximately as follows:
For the 10% group
| Strawberry jam: Approximately 32.73 grams |
| Chocolate candy bar: Approximately 15.11 grams |
| Chocolate biscuit bar: Approximately 12.09 grams |
| Yogurt with fruit purée: Approximately 10.07 grams |
| Sugar: 10 grams (fixed value) |
| Total 80g |
For the 25% group
| Smartie-type sweets: Approximately 40.77 grams |
| Milk chocolate: Approximately 27.23 grams |
| Orange Juice: Approximately 24.02 grams |
| Vanilla fudge: Approximately 23.30 grams |
| Pineapple Juice: Approximately 18.20 grams |
| Apple: 18 grams |
| Chocolate nut bar: Approximately 17.47 grams |
| Yogurt with fruit purée: Approximately 16.02 grams |
| Direct sugar: 15 grams (fixed value) |
| Total 200g |
That gives us a fruit-adjusted free sugar to total intake of 15% for the 25% group, and 5% for the 10% group, both are within the range according to them:
The American Heart Association adopted a similar approach commenting on the potential detrimental effects of a high-sucrose content diet with expected adverse effects when content exceeded >20% of total energy intake (28). Such effects included a fall in HDL levels, a rise in triglycerides, and decreased vitamin and mineral content. In the U.K., the Department of Health recently suggested reducing mean added sugar intake from 12.7 to 11%
The authors missed the most important measures of insulin resistance, hyperinsulinemia:
Furthermore, although 24-h glycemic profiles and insulin clearance were similar on the high- and low-sucrose diets, we did not directly assess insulin secretion or postprandial metabolic changes. It is, however, possible that a high-sucrose diet could have detrimental effects on insulin secretion and postprandial glucose and lipid metabolism, particularly in established type 2 diabetes where these are recognized to be important features.
The authors did acknowledge the statistical significance of the rise in LDL, despite the short period of the study and lack of statistical power of the sample size.
A rise in total and LDL cholesterol and a trend toward increased triglycerides were observed during the 25% sucrose diet compared with the 10% sucrose diet. Although the mean changes were relatively modest and levels remained within normal ranges, it is possible that more marked abnormalities could arise in subjects with hyperlipidemia at baseline. Other studies have demonstrated increased triglyceride levels with sucrose contents >20%; however, the LDL increase is more unusual (46). A similar change in lipoprotein profiles has been noted in high-fructose diets in man (47).
Moreover, the calories were not macro-equivalent, the more metabolically detrimental PUFA was assigned to the lower sucrose group
Fructose is the more lipogenic component, as it bypasses a major rate-controlling step in glycolysis (48). The food selection that was necessary to achieve the balance resulted in a change in fat quality but no change in total fat quantity. The high-sucrose diet had 29% higher energy content from saturated fat and 29% lower polyunsaturated fat than the low-sucrose diet.
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Have you not read anything I've said before?
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Hi Haidut,Not true. Sugar ("refined cane and beet sugar" in the graph below) consumption has been steadily decreasing since the 1970s and is currently at its lowest level ever, while obesity rates have skyrocketed since the 1970s and have not had even a single year or flattening/reversal.
The Dose Makes the Poison: Sugar and Obesity in the United States – a Review
Two-thirds of the US population is either overweight or obese. Obesity is one of the major drivers of preventable diseases and health care costs. In the US, current estimates for these costs range from $147 to $210 billion per year. Obesity is a multifactorial ...
In fact, even if you look at total carb (sugar + other types) consumption. the rate per capita in the US is at the levels of 1970-1980s (see above link), and in 1975 the obesity rate was 10%-12% while now it is ~40% (see below).
Obesity in the United States - Wikipedia
en.wikipedia.org
So, sucrose consumption and obesity rates would be very strongly negatively correlated if one were to use those curves shown in the graphs above. Furthermore, if you look at rates for cancer, CVD, dementia, Parkinson, etc you will see that those have also been rising since 1975 and overlap almost perfectly with the rise in obesity rates, and inversely correlated with sugar consumption. Worse, the mortality from the major chronic diseases has also been rising since the 1970s and shows no sign of abating.
The Top 3 Causes of Diabetes | The Motley Fool
Affecting more than 25 million people in the U.S., here are the primary factors that lead to this potentially debilitating disease and what's being done to curb its growth.www.fool.com
Infographic: Alzheimer’s Is Becoming More Prevalent
This chart shows the number of deaths from Alzheimer's disease per 100,000 people in the United States between 2000 and 2019.www.statista.com
@Peatful
I've addressed this in post #17, but I have not posted the study. Age adjusted obesity according to generation of sugar consumption model explains it well. The authors suggest early exposure to high or low consumption dictates life-long outcomes for obesity more powerfully than a dietary change in adults.
In summary, we have modeled the recent increase of U.S. adult obesity rates since the 1990s as a legacy of increased consumption of excess sugars among children of the 1970s and 1980s. Our model proposes, for each age cohort, that the current obesity rate will be the obesity rate in the previous year plus a simple function of the mean excess sugar consumed in the current year. With just these inputs, the model can replicate the timing and magnitude of the national rise in obesity, as well as the profile of obesity rates by age group, and the different patterns of change in obesity among children and adolescent age group, where reduction in obesity registered first among young children in the late 1990s. This supports the perspective that the rise in U.S. adult obesity after 1990 was a generation-delayed effect of the increase in excess sugar calories consumed among children of the 1970s and 1980s.
I am personally not a fan of using population level retrospective univariable data given the thousands of possible confounding factors. Who knows what else had an explanatory power, like less activity, more time indoors, more affordable food.
I agree with that, but it is hard to argue that it is the sugar consumption per as the primary course/cause of modern diseases (as the title of the thread says), when the consumption curves and disease rates are exact opposites of each other. There are plenty of other variables with plausibly stronger causative effect, proven with randomized controlled trials - i.e. contraception in women, SSRI drugs, statins, PPI drugs, etc.
The fraud unravels - statins cause, not prevent heart disease (CVD)
While the news that the statin fraud is finally being exposed is certainly good, it is sad that it took so many decades to admit to something so biochemically obvious. Namely, since statins interfere with the synthesis of mevalonic acid, as a consequence they also inhibit the synthesis of the...
As others responded earlier, any of the links between sucrose consumption and chronic disease can be explained by endotoxemia, of which sucrose is a more or less an innocent bystander, consumed on top of an already high fat (PUFA) diet. Low-fat, high-sucrose diets cause neither obesity, nor chronic diseases in animal models. In fact, such diets extend maximum lifespan in some species studies so far.
Bacterial Lipids (endotoxin), Not Cholesterol, May Be A Cause Of CVD
The role of endotoxin (and TLR) in cardiovascular disease (CVD) is probably well-known by most people on this forum. Peat rarely writes on a topic without mentioning either endotoxin or keeping the gut clean as one of the main paths to good health. The role of cholesterol is finally getting to...
I don’t think it can get more clear to be honest. It’s a randomized control trial, which is the highest level of causal evidence available. Both groups were placed on nearly identical eucaloric diets, with the experimental group having a 15% higher sucrose intake. This resulted in no significant difference in insulin sensitivity or glycemic profile.
As for this response, it’s a eucaloric or weight maintaining diet study, so speculating on the calories needed for the participants to maintain weight doesn’t really make sense. Besides that, the difference in fat mass still isn’t significantly different, which is generally the standard of evidence to conclude that there is a correlation(not to mention causation, which can only really be concluded by randomized control trials).
Here’s another:
“These studies suggest that fructose, when consumed at levels consumed by up to 90% of the population in the common sucrose and HFCS sweeteners, does not result in increased liver fat or intramuscular adipose tissue accumulation. These data raise questions about the quantitative significance of de novo lipogenesis in response to normally consumed levels of fructose in the human diet. Further studies with a larger sample size, longer duration, and adolescents appear to be warranted.”
It seems relatively clear that when sucrose is consumed at human relevant levels as part of a eucaloric diet, it does not lead to increased insulin resistance or increased adipogenesis in the liver and/or elsewhere in the body.
“These studies suggest that fructose, when consumed at levels consumed by up to 90% of the population in the common sucrose and HFCS sweeteners, does not result in increased liver fat or intramuscular adipose tissue accumulation. These data raise questions about the quantitative significance of de novo lipogenesis in response to normally consumed levels of fructose in the human diet. Further studies with a larger sample size, longer duration, and adolescents appear to be warranted.”
It seems relatively clear that when sucrose is consumed at human relevant levels as part of a eucaloric diet, it does not lead to increased insulin resistance or increased adipogenesis in the liver and/or elsewhere in the body.
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Another:
www.frontiersin.org
“In our study, we showed that lifelong consumption of a diet consisting of 25% kcal from sucrose generally had no significant impact on inducing overeating and obesity and most related outcomes (blood glucose and insulin level; plasma total cholesterol and TG level; liver histopathology and gene expression; and life expectancy), compared to a 10% kcal sucrose diet. To the best of our knowledge, there are no previous studies that examined the health effects of chronic higher sugar intake on metabolic and endocrine health. The null findings of our study thus disagree with conclusions from previous animal studies that high sugar intake causes obesity and related complications. Our data presented here suggest further pre-clinical and human studies to elucidate and confirm the effects of chronic intake of sucrose at human-relevant levels are required to better inform the dietary guidelines and public health policy development on sugar consumption.”
Effect of lifelong sucrose consumption at human-relevant levels on food intake and body composition of C57BL/6N mice
IntroductionControversies surround the issue if chronic consumption of a high-sugar diet is detrimental to health or not. This study investigates whether lifelong consumption of a higher sucrose diet will induce overeating, and obesity, and cause metabolic dysfunctions such as hyperglycemia and...
“In our study, we showed that lifelong consumption of a diet consisting of 25% kcal from sucrose generally had no significant impact on inducing overeating and obesity and most related outcomes (blood glucose and insulin level; plasma total cholesterol and TG level; liver histopathology and gene expression; and life expectancy), compared to a 10% kcal sucrose diet. To the best of our knowledge, there are no previous studies that examined the health effects of chronic higher sugar intake on metabolic and endocrine health. The null findings of our study thus disagree with conclusions from previous animal studies that high sugar intake causes obesity and related complications. Our data presented here suggest further pre-clinical and human studies to elucidate and confirm the effects of chronic intake of sucrose at human-relevant levels are required to better inform the dietary guidelines and public health policy development on sugar consumption.”
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Alright, I think I know what I'm dealing with here.
Study significantly underpowered, subjects in a group in single digits, even if there was a statistically significant effect, it wouldn't show up.
You seem to be strongly intent on defending the multi-billion dollar sugar industry for some reason, why is that?
The authors thank the staff of Rippe Lifestyle Institute and Sand Lake Imaging for their expertise in conducting this study. We also thank Elizabeth Grady and Noy Supaswud for their assistance in the generation of this manuscript and Teresa Bravo for her help in data handling related to CT and MRI scans. Steve Bravo has received consulting fees and equipment support from Siemens Inc. James M. Rippe's research organization has received funding, and Dr. Rippe has received consulting fees, from ConAgra Foods, PepsiCo International, Kraft Foods, the Corn Refiners Association, and Weight Watchers International.
Please leave my thread, I think we know who you really are.
To get that message out, the campaign relies on nutritional research. But CBS News has learned that funding for many of the major studies came from companies with a financial stake in the outcome.
Of the six studies CBS News looked at on the association's Web site that "Confirm High Fructose Corn Syrup [is] No Different From Sugar," three were sponsored by groups that stand to profit from research that promotes HFCS. Two were never published so their funding sources are unclear. And one was sponsored by a Dutch foundation that represents the interests of the sugar industry.
Pepsi funded one study, so did a D.C. based lobbying group that gets their money from food, chemical and drug companies. And the American Beverage Association gave a grant for another.
One researcher who was involved in three of the studies, Dr. James M. Rippe, a cardiologist and founder of the Rippe Lifestyle Institute says there is no link between HFCS and obesity and calls contrary evidence "accusations" and "speculation."
Rippe's ties with industry are no secret. Pepsico, Tropicana and Quaker among others are all listed as Rippe Health Partners on his Web site along with this quote: "The RLI research team conducts multiple studies of mutual interest to RLI and PepsiCo North America in topics such as short-term energy regulation response to high fructose corn syrup…"
But research indicates the source of a study's funding has a stake in the outcome.
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