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Blood Glucose, Curcumin, Sugar, And Coffee

October 2017

Sugar

Sugar Industry and Coronary Heart Disease Research: A Historical Analysis of Internal Industry Documents.

Early warning signals of the coronary heart disease (CHD) risk of sugar (sucrose) emerged in the 1950s. We examined Sugar Research Foundation (SRF) internal documents, historical reports, and statements relevant to early debates about the dietary causes of CHD and assembled findings chronologically into a narrative case study. The SRF sponsored its first CHD research project in 1965, a literature review published in the New England Journal of Medicine, which singled out fat and cholesterol as the dietary causes of CHD and downplayed evidence that sucrose consumption was also a risk factor. The SRF set the review's objective, contributed articles for inclusion, and received drafts. The SRF's funding and role was not disclosed. Together with other recent analyses of sugar industry documents, our findings suggest the industry sponsored a research program in the 1960s and 1970s that successfully cast doubt about the hazards of sucrose while promoting fat as the dietary culprit in CHD. Policymaking committees should consider giving less weight to food industry-funded studies and include mechanistic and animal studies as well as studies appraising the effect of added sugars on multiple CHD biomarkers and disease development.

JAMA Intern Med. 2016 Nov 1;176(11):1680-1685.

Sugar industry influence on the scientific agenda of the National Institute of Dental Research's 1971 National Caries Program: a historical analysis of internal documents.

BACKGROUND: In 1966, the National Institute of Dental Research (NIDR) began planning a targeted research program to identify interventions for widespread application to eradicate dental caries (tooth decay) within a decade. In 1971, the NIDR launched the National Caries Program (NCP). The objective of this paper is to explore the sugar industry's interaction with the NIDR to alter the research priorities of the NIDR NCP. METHODS AND FINDINGS: We used internal cane and beet sugar industry documents from 1959 to 1971 to analyze industry actions related to setting research priorities for the NCP. The sugar industry could not deny the role of sucrose in dental caries given the scientific evidence. They therefore adopted a strategy to deflect attention to public health interventions that would reduce the harms of sugar consumption rather than restricting intake. Industry tactics included the following: funding research in collaboration with allied food industries on enzymes to break up dental plaque and a vaccine against tooth decay with questionable potential for widespread application, cultivation of relationships with the NIDR leadership, consulting of members on an NIDR expert panel, and submission of a report to the NIDR that became the foundation of the first request for proposals issued for the NCP. Seventy-eight percent of the sugar industry submission was incorporated into the NIDR's call for research applications. Research that could have been harmful to sugar industry interests was omitted from priorities identified at the launch of the NCP. Limitations are that this analysis relies on one source of sugar industry documents and that we could not interview key actors. CONCLUSIONS: The NCP was a missed opportunity to develop a scientific understanding of how to restrict sugar consumption to prevent tooth decay. A key factor was the alignment of research agendas between the NIDR and the sugar industry. This historical example illustrates how industry protects itself from potentially damaging research, which can inform policy makers today. Industry opposition to current policy proposals-including a World Health Organization guideline on sugars proposed in 2014 and changes to the nutrition facts panel on packaged food in the US proposed in 2014 by the US Food and Drug Administration-should be carefully scrutinized to ensure that industry interests do not supersede public health goals.

PLoS Med. 2015 Mar 10;12(3):e1001798.

Global and regional mortality from ischaemic heart disease and stroke attributable to higher-than-optimum blood glucose concentration: comparative risk assessment.

Cardiovascular mortality risk increases continuously with blood glucose, from concentrations well below conventional thresholds used to define diabetes. We aimed to quantify population-level effects of all higher-than-optimum concentrations of blood glucose on mortality from ischaemic heart disease and stroke worldwide. METHODS: We used population distribution of fasting plasma glucose to measure exposure to higher-than-optimum blood glucose. We collated exposure data in 52 countries from individual-level records in population health surveys, systematic reviews, and data provided by investigators. Relative risks for ischaemic heart disease and stroke mortality were from a meta-analysis of more than 200,000 participants in the Asia-Pacific region, with adjustment for other cardiovascular risk factors. RESULTS: In addition to 959,000 deaths directly assigned to diabetes, 1,490,000 deaths from ischaemic heart disease and 709,000 from stroke were attributable to high blood glucose, accounting for 21% and 13% of all deaths from these conditions. 1.8 million of these 2.2 million cardiovascular deaths (84%) were in low-and-middle-income countries (1,224,000 for ischaemic heart disease, 623,000 for stroke). 792,000 (53%) of deaths from ischaemic heart disease and 345,000 (49%) from stroke that were attributable to high blood glucose were in men. Largest numbers of deaths attributable to this risk factor from ischaemic heart disease were in low-and-middle-income countries of South Asia (548,000) and Europe and Central Asia (313,000), and from stroke in South Asia (215,000) and East Asia and Pacific (190,000). INTERPRETATION: Higher-than-optimum blood glucose is a leading cause of cardiovascular mortality in most world regions. Programmes for cardiovascular risk and diabetes management and control at the population level need to be more closely integrated.

Lancet. 2006 Nov 11;368(9548):1651-9.

Chronic hyperglycemia impairs endothelial function and insulin sensitivity via different mechanisms in insulin-dependent diabetes mellitus.

BACKGROUND: We explored whether chronic hyperglycemia is associated with defects in endothelium-dependent vasodilatation in vivo and whether defects in the hemodynamic effects of insulin explain insulin resistance. METHODS AND RESULTS: Vasodilator responses to brachial artery infusions of acetylcholine, sodium nitroprusside, and NG-monomethyl-L-arginine and, on another occasion, in vivo insulin sensitivity (euglycemic insulin clamp combined with the forearm catheterization technique) were determined in 18 patients with insulin-dependent diabetes mellitus (IDDM) and 9 normal subjects. At identical glucose and insulin levels, insulin stimulation of whole-body and forearm glucose uptake was 57% reduced in the IDDM patients compared with normal subjects (P < .001). The defect in forearm glucose uptake was attributable to a defect in glucose extraction (glucose AV difference, 1.1 +/- 0.2 versus 1.9 +/- 0.2 mmol/L, P < .001, IDDM versus normal subjects), not blood flow. Within the group of IDDM patients, hemoglobin A1c was inversely correlated with forearm blood flow during administration of acetylcholine (r = -.50, P < .02) but not sodium nitroprusside (r = .07). The ratio of endothelium-dependent to endothelium-independent blood flow was approximately 40% lower in patients with poor glycemic control than in normal subjects or patients with good or moderate glycemic control. CONCLUSIONS: We conclude that chronic hyperglycemia is associated with impaired endothelium-dependent vasodilatation in vivo and with a glucose extraction defect during insulin stimulation. These data imply that chronic hyperglycemia impairs vascular function and insulin action via distinct mechanisms. The defect in endothelium-dependent vasodilatation could contribute to the increased cardiovascular risk in diabetes.

Circulation. 1996 Sep 15;94(6):1276-82.

Advances in biochemical mechanisms of diabetic retinopathy.

Diabetes mellitus is a major cause of blindness in the working population of the Western World. Numerous large, prospective, randomized clinical trials have delineated the current standard prevention and treatment protocols including intensive glycemic and blood pressure control as well as laser photocoagulation for clinically significant macular edema and/or proliferative retinopathy at a high risk for tractional retinal detachment. However, despite all these interventions, vision loss from diabetic retinopathy still occurs at an alarming rate and no data provide an adequate explanation for the serious and rapid involvement of the retinal microcirculation that may be observed in the disease despite a good metabolic control. In fact, there is now ample of evidence that the development of diabetic retinopathy is a multifactorial process where genetic, metabolic and growth factors play an important role. Some biochemical mechanisms, supposed to be involved in the pathogenesis of diabetic retinopathy, have been highlighted in this review.

Eur Rev Med Pharmacol Sci. 2007 May-Jun;11(3):155-63.

Advanced glycation endproducts in human diabetic and non-diabetic cataractous lenses.

BACKGROUND: Advanced glycation endproduct (AGE) formation is thought to contribute to aging and cataract formation in the lens. In this study, we evaluated AGE immunoreactivity in human diabetic (n=14) and nondiabetic (n=31) cataractous lenses in relation to high-molecular-weight (HMW) protein content, which is believed to contribute to the onset of cataract. METHODS: AGE immunoreactivity was detected in alkali-soluble individual lens samples. Competitive ELISA with polyclonal anti-AGE antibody was performed to estimate AGEs. SDS-PAGE was used to detect changes in lens protein composition on the basis of molecular size. RESULTS: Regression analysis of data from nondiabetic lenses showed a significant correlation between lens AGE content and patient age (r=0.665, P<0.001). The curve exhibited exponential regression ( y=0.272.e(0.025x)). The level of nonspecified AGEs measured in diabetic lenses showed an overall increase compared with nondiabetic lenses (4.03+/-1.85 vs 1.78+/-0.71 AU/mg protein, P<0.0078). SDS-PAGE showed the occurrence of HMW proteins in both diabetic and nondiabetic lens samples. However, in diabetic patients, who had a higher level of AGEs, a significantly higher proportion of HMW proteins was also observed. The levels of AGE and percent of HMW aggregates showed a very significant correlation ( r=0.68, P<0.007) in the diabetic group, whereas in nondiabetics the correlation, although positive, did not reach statistical significance.CONCLUSION: The AGE distribution, with a higher proportion in the samples of lenses rich in HMW aggregates, corroborates the hypothesis that the advanced glycation process might have a role in degenerative changes in eye lens, which in diabetic patients occur vigorously and much earlier than in those without diabetes.

Graefes Arch Clin Exp Ophthalmol. 2003 May;241(5):378-84.

Low to moderate sugar-sweetened beverage consumption impairs glucose and lipid metabolism and promotes inflammation in healthy young men: a randomized controlled trial.

BACKGROUND: Sugar-sweetened beverages (SSBs) have unfavorable effects on glucose and lipid metabolism if consumed in high quantities by obese subjects, but the effect of lower doses in normal-weight subjects is less clear. OBJECTIVE: The aim was to investigate the effects of SSBs consumed in small to moderate quantities for 3 wk on LDL particle distribution and on other parameters of glucose and lipid metabolism as well as on inflammatory markers in healthy young men. DESIGN: Twenty-nine subjects were studied in a prospective, randomized, controlled crossover trial. Six 3-wk interventions were assigned in random order as follows: 600 mL SSBs containing 1)40 g fructose/d [medium fructose (MF)], 2) 80 g fructose/d [high fructose (HF)], 3) 40 g glucose/d [medium glucose (MG)], 4) 80 g glucose/d [high glucose (HG)], 5) 80 g sucrose/d [high sucrose (HS)], or 6) dietary advice to consume low amounts of fructose. Outcome parameters were measured at baseline and after each intervention. RESULTS: LDL particle size was reduced after HF by -0.51 nm (95% CI: -0.19, -0.82 nm) and after HS by -0.43 nm (95% CI: -0.12, -0.74; P < 0.05 for both). Similarly, a more atherogenic LDL subclass distribution was seen when fructose-containing SSBs were consumed (MF, HF, and HS: P < 0.05). Fasting glucose and high-sensitivity C-reactive protein (hs-CRP) increased significantly after all interventions (by 4-9% and 60-109%, respectively; P < 0.05); leptin increased during interventions with SSBs containing glucose only (MG and HG: P < 0.05). CONCLUSION: The present data show potentially harmful effects of low to moderate consumption of SSBs on markers of cardiovascular risk such as LDL particles, fasting glucose, and hs-CRP within just 3 wk in healthy young men, which is of particular significance for young consumers.

Am J Clin Nutr. 2011 Aug;94(2):479-85.