There is no threshold for healthy blood glucose:
Is there a glycemic threshold for mortality risk?
Diabetes Care May 1999 vol. 22 no. 5 696-699
“…the lowest observed death rates were in the intervals centered on 5.5 mmol/l [99mg/dl] for fasting glucose and 5.0 mmol/l [90 mg/dl] for 2-h glucose.
CONCLUSIONS: In the Paris Prospective Study, there were no clear thresholds for fasting or 2-h glucose concentrations above which mortality sharply increased; in the upper levels of the glucose distributions, the risk of death progressively increased with increasing fasting and 2-h glucose concentrations.”
“Normal” blood glucose and coronary risk
BMJ VOLUME 322 6 JANUARY 2001
“Khaw et al in this issue shows that glycosylated haemoglobin levels are positively associated with the risk of future coronary heart disease in a linear stepwise fashion, with no evidence of a threshold effect and independent of other common risk factors for coronary heart disease. These are the most convincing data available that the association between glucose and coronary heart disease occurs throughout the normal range of glucose.”
Post-challenge blood glucose concentration and stroke mortality rates in non-diabetic men in London: 38-year follow-up of the original Whitehall prospective cohort study
Diabetologia (2008) 51:1123–1126
“Results During follow-up of 18,406 non-diabetic men, 13,116 deaths occurred (1,189 by stroke).
Plots of stroke mortality rates versus [post challenge of 50 gms] blood glucose identified an upward inflection in risk of death from stroke at about 4.6 mmol/l [82 mg/dl]. This upward inflection in risk could be adequately described using a single linear term above this threshold. Conclusions/interpretation; An incremental elevation in stroke mortality rates occurs with increasing post-challenge blood glucose.”
2010 WebMD
How the Blood Sugar of Diabetes Affects the Body
“At present, the diagnosis of diabetes or prediabetes is based on an arbitrary cut-off point for a normal blood sugar level.”
ScienceDaily, Monash University (2008, August 22)
Killer Carbs: Scientist Finds Key To Overeating As We Age
published in ‘Nature’.
“Dr Andrews found that appetite-suppressing cells are attacked by free radicals after eating and said the degeneration is more significant following meals rich in carbohydrates and sugars. ‘The more carbs and sugars you eat, the more your appetite-control cells are damaged, and potentially you consume more,’ Dr Andrews said.”
Is There a Clear Threshold for Fasting Plasma Glucose That Differentiates
Between Those With and Without Neuropathy and Chronic Kidney Disease?
Am J Epidemiol 2009;169:1454–1462
“Recent studies suggest that no distinct glycemic threshold consistently differentiates individuals with or without retinopathy. The authors sought to determine whether the same was true [in a random sample of individuals] for other microvascular complications…Prevalence of peripheral neuropathy and chronic kidney disease gradually increased in relation to fasting plasma glucose, beginning at levels below the existing diagnostic threshold for diabetes mellitus of 7.0 mmol/L (126 mg/dL).”
One-hour postload plasma glucose and risks of fatal coronary heart disease and stroke among nondiabetic men and women: the Chicago Heart Association Detection Project in Industry (CHA) Study.
J Clin Epidemiol. 1997 Dec;50(12):1369-76
Stamler J. Northwestern University Medical School, Chicago, IL
“Plasma glucose was determined one hour after a 50-gram oral glucose load… higher glucose was significantly associated with mortality from coronary heart disease, stroke, cardiovascular diseases, and all cause mortality in men and women. This large longitudinal study provides evidence that one-hour postload plasma glucose in the absence of clinical diabetes at baseline apparently is an independent risk factor for fatal coronary heart disease and stroke in middle-aged and older nondiabetic men and women, and also for cardiovascular diseases and for all cause mortality.”
Glycated haemoglobin, diabetes, and mortality in men in Norfolk cohort of European Prospective Investigation of Cancer and Nutrition (EPIC°©Norfolk)
BMJ VOLUME 322 6 JANUARY 2001
“HbA1c was continuously related to subsequent all cause, cardiovascular, and ischaemic heart disease mortality through the whole population distribution, with lowest rates in those with HbA1c concentrations below 5%. An increase of 1% in HbA1c was associated with a 28% (P < 0.002) increase in risk of death..."
Glucose accelerates aging, oxidative stress…
Pro-Aging Effects of Glucose Signaling through a G Protein-Coupled Glucose Receptor in Fission Yeast
PLoS Genetics, March 2009 | Volume 5 | Issue 3
“…excess of glucose has been associated with several diseases, including diabetes and the less understood process of aging. On the contrary, limiting glucose (i.e., calorie restriction) slows aging and age-related diseases in most species…The pro-aging effect of glucose signaling on life span correlated with an increase in reactive oxygen species and a decrease in oxidative stress resistance and respiration rate. Likewise, the anti-aging effect of both calorie restriction and the Dgit3 mutation was accompanied by increased respiration and lower reactive oxygen species production.”
Rather than being good for white blood cells, glucose can oxidize them…
GLUCOSE CHALLENGE STIMULATES REACTIVE OXYGEN SPECIES (ROS) GENERATION BY LEUCOCYTES
The Journal of Clinical Endocrinology & Metabolism, Vol. 85, No. 8, Aug. 2000
“Blood samples were drawn from 14 normal subjects prior to, at 1, 2 and 3 h following ingestion of 75 g glucose…We conclude that glucose intake…increases oxidative load [in leukocytes] and causes a fall in a-tocopherol concentration.”
Sugar glycates. For those unaware, this is where glucose (and other sugars) combines with other essential molecules such as proteins and DNA affecting their shape and structure and preventing their proper function. This is a very bad. Glycation is one of the major molecular mechanisms that cause damage resulting in senescence that we notice as “aging”. That is why products of glycation, advanced glycated end products, are not coincidentally called AGEs.
There is no threshold for glycation…more glucose, greater risk of glycation…
Advanced glycated end products: a review
Diabetologia (2001) 44: 129-146
“Glycation is concentration-dependent”
Lipoprotein Lipase Mediates the Uptake of Glycated LDL in Fibroblasts, Endothelial Cells, and Macrophages.
Diabetes 50: 1643–1653, 2001
“Protein glycation is a nonenzymatic reaction of glucose with susceptible amino groups that occurs at a rate linearly related to the plasma glucose concentration.”
Significant amounts of highly reactive precursors to AGEs (advanced glycated end products) are formed after a single standard (with carbohydrate) meal…
a-Dicarbonyls Increase in the Postprandial Period and Reflect the Degree of Hyperglycemia.
Diabetes Care 24:726–732, 2001
“Chronic hyperglycemia is known to increase tissue glycation and diabetic
complications, but controversy exists regarding the independent role of increased postprandial glucose excursions. To address this question, we have studied the effect of postprandial glycemic excursions (PPGEs) on levels of methylglyoxal (MG) and 3-deoxyglucosone (3-DG), two highly reactive precursors of advanced glycation end products (AGEs)….PPGE was determined after a standard test meal. Conclusion: Increased production of MG and 3-DG [AGEs] occur with greater PPGE, whereas HbA1c does not reflect these differences.”
Insulin glycates contributing to insulin resistance…and its sequelae, diabetes, CV disease, obesity, cancer, and accelerated aging…
Glycation of insulin results in reduced biological activity in mice.
Acta Diabetol. 1997 Dec;34(4):265-70
“These data indicate that glycated insulin exhibits impaired biological activity which may contribute to glucose intolerance…”
Glycation of LDL in non-diabetic people: Small dense LDL is preferentially
glycated both in vivo and in vitro.
Atherosclerosis. 2009 Jan;202(1):162-8
“CONCLUSION: Small-dense LDL is more susceptible to glycation and this may contribute to the atherogenicity of smalldense LDL, even in non-diabetic people.”
Glucose directly contributes to aging and feeds cancer cells;
Glucose restriction can extend normal cell lifespan and impair precancerous cell growth through epigenetic control of hTERT and p16 expression.
FASEB, December 17, 2009
“Cancer cells metabolize glucose at elevated rates and have a higher sensitivity to glucose reduction…The altered gene expression was partly due to glucose restriction-induced DNA methylation changes…Collectively, these results provide new insights into the epigenetic mechanisms of a nutrient control strategy that may contribute to cancer therapy as well as antiaging approaches.”
Raising glucose, raises insulin, increases insulin resistance…
Beta-cell dysfunction and glucose intolerance: results from the San Antonio metabolism (SAM) study.
Diabetologia (2004) 47:31–39
“Conclusion/interpretation. When the plasma insulin response to oral glucose is related to the glycaemic stimulus and severity of insulin resistance, there is a progressive decline in beta-cell function that begins in “normal” glucose tolerant individuals.”
out:, but the thought that I might not have to give up *all* the things I enjoy on a frequent basis (the homemade smoothies I make for breakfast or lunch for the whole family when things are rushed) and coffee with real sugar and 1/2 & 1/2 is a great comfort to me at the moment. I used to drink 2 or 3 extra-large mugs of coffee a day. Yesterday and today I have limited it to 1. I need to lose weight and since it's such a high carb item I want to moderate. As a cancer survivor, I do not ever consume artificial sweeteners, and I don't like the taste of Stevia at all. So I either put sugar in my coffee or I drink it black. I strongly prefer the sugar, but not enough to die or damage my organs for.
