Life Extension Magazine®

Critical Need to Control Fasting and After-Meal Glucose Levels

Life Extension® members have known for years that keeping a tight rein on fasting glucose levels is a cornerstone strategy for increasing healthy life span. Now, compelling new findings from an organization called Living the CR Way suggest that low fasting glucose favorably infl uences our longevity genes!

Scientifically reviewed by Dr. Gary Gonzalez, MD, in October 2024. Written by: William Faloon.

Critical Need to Control Fasting and After-Meal Glucose Levels

We at Life Extension® have a unique mission. We strive to keep our members alive and in good health for an indefinite time period.

Enough data has accumulated over the past decade for us to make a firm recommendation that all Life Extension® members take aggressive steps to suppress their fasting glucose levels to around 80 (mg/dL) of blood.

This suggestion is not new, as we long ago published findings from scientific studies revealing that mainstream medicine was accepting dangerously high levels of fasting glucose as being “normal.”

What is different now are compelling arguments from an organization called Living the CR Way stating that keeping tight control over glucose not only protects against common diseases, but also favorably influences genes that control our rate of aging.

So far in this issue of Life Extension Magazine®, you have learned about nutritional and pharmaceutical approaches that have been shown to suppress blood glucose levels. These include a new Calorie Control Weight Management nutrient powder that should be taken before the two largest meals of the day.

This article describes the scientific rationale for keeping fasting glucose levels at around 80 mg/dL (or lower) and postprandial (after meal) glucose levels that increase no more than 40 mg/dL before dropping back to fasting ranges in the 80s.

The section after describes how you can adopt a lower calorie diet that can be followed for a lifetime to achieve optimal glucose control.

Lethal Consequences of Excess Glucose

Lethal Consequences of Excess Glucose

Blood glucose levels play a crucial role in determining how long you will live. High blood glucose, either fasting or postprandial (after the meal) is a risk factor for diabetes, heart disease, cancer, and Alzheimer’s disease as well as increased mortality. In fact, high glucose levels are such a threat to public health that San Francisco has declared a “Soda-free Summer”– realizing that sugar-loaded sodas fuel glucose levels, helping to cause the diabetes epidemic that plagues the city. Other areas of the country are considering similar measures.

The dangers of high glucose are so strongly supported by research findings that the International Diabetes Federation has issued a warning to non-diabetics that postprandial (after meal) glucose above 140 mg/dL is a significant risk factor1 for many diseases including:

  • Damage to the retina
  • Increased intima-media thickness of the carotid artery
  • Oxidative stress
  • Increased inflammation
  • Endothelial dysfunction
  • Decreased myocardial blood flow
  • Increased cancer risk

The Living The CR Way program recommends keeping a tight rein on postprandial glucose–aiming to keep meals from raising blood glucose more than 40 mg/dL: This often results in postprandial blood glucose of 120 mg/dL or less.

Keeping Glucose Low Essential for Optimal Health

Lethal Consequences of Excess Glucose

If high glucose is a risk factor, could keeping glucose low provide benefits? Yes! Keeping glucose low is important for everyone who cares about their health. It is also a cornerstone of calorie restriction—now proven to produce profound benefits in humans.2-6 Glucose is the preferred fuel for cellular metabolism, but when calories are limited by a healthful and nutrient-dense diet whose components have low GI (glycemic index) rankings, glucose levels fall as blood sugar is used up quickly for the body’s countless processes. Indeed, the fasting glucose levels of the cohort of serious, long-term calorie restrictors participating in the studies at Washington University Medical School were well-controlled between 74 and 88 mg/dL.7

Calorie restrictors should aim for fasting glucose levels in the 80s or below.8 When glucose falls into the 80s or below, profound physiological changes take place. The body shifts gears–burning fat and protein for energy. A beneficial regulator controlling this metabolic switch is AMPK (AMP-activated protein kinase), an enzyme that regulates glucose and lipid metabolism. Its actions include facilitation of glucose transport into muscle cells, protection against ischemic heart disease, and decreasing the liver’s production of glucose, cholesterol, and triglycerides. AMPK also powers the beneficial actions of the popular diabetes drug, metformin.9

When a cell’s energy state diminishes, AMPK becomes active10 and works in concert with the fuel-sensing gene, SIRT,11 which plays a role in the longevity and related benefits of calorie restriction, including reduced inflammation and better mitochondrial function.

“Keeping glucose low enough to activate the beneficial effects of CR is important for everyone, whether they consider themselves calorie-restricted or not,” says Paul McGlothin,12 Vice President for Research of the CR Society Intl. and co-author of The CR Way book that many Life Extension members already have.

Activation of AMPK and its partner SIRT1 causes the fat-forming genetic complex PPAR-gamma (peroxisome proliferator-activated receptor-gamma) to be blocked,13 and the body to shift from fat storage to fat burning.

This is great news for anyone who wants to lose weight: the pounds burn away quickly when the fat-forming genes have been blocked. This also benefits cardiovascular health: fat that otherwise might end up as artery plaque is simply burned for fuel.

The next article describes aggressive ways to implement a personal calorie restriction program.

If you have any questions on the scientific content of this article, please call a Life Extension® Health Advisor at
1-866-864-3027.

Continued on Calorie Restriction Can Be Easy!

References

1. Available at: http://www.idf.org/webdata/docs/Guideline_PMG_final.pdf . Accessed July 27, 2010

2. McGlothin P. The New Calorie Restriction—For Optimal Health and Happiness. Presented at: Aging and Healthy Lifespan Conference. Harvard Medical School; September, 2009.

3. Fontana L, Meyer TE, Klein S, Holloszy JO. Long-term calorie restriction is highly effective in reducing the risk for atherosclerosis in humans. Proc Natl Acad Sci U S A. 2004 Apr 7; 101(17):6659-63.

4. Meyer TE, Kovacs SJ, Ehsani AA, Klein S, Holloszy JO, Fontana L. Long-term caloric restriction ameliorates the decline in diastolic function in humans. J Am Coll Cardiol. 2006 Jan 17;47(2):398-402.

5. Fontana L, Klein S, Holloszy JO, Premachandra BN. Effect of long-term calorie restriction with adequate protein and micronutrients on thyroid hormones. J Clin Endocrinol Metab. 2006 Aug;91(8):3232-5.

6. Fontana L, Klein S. Aging, adiposity, and calorie restriction. JAMA. 2007 Mar 7;297(9):986-94.

7. Fontana L. The scientific basis of caloric restriction leading to longer life. Curr Opin Gastroenterol. 2009 Mar;25(2):144-50.

8. McGlothin P, Averill M. Glucose Control: The Sweet Spot in Longevity. In: McGlothin P, Averill M. The CR Way: Using the Secrets of Calorie Restriction for a Longer, Healthier Life. New York, NY: HarperCollins; 2008: 57-78.

9. Misra P, Chakrabarti R. The role of AMP kinase in diabetes. Indian J Med Res. 2007 Mar;125(3):389-98

10. Cai F, Gyulkhandanyan AV, Wheeler MB, Belsham DD. Glucose regulates AMP-activated protein kinase activity and gene expression in clonal, hypothalamic neurons expressing proopiomelanocortin: additive effects of leptin or insulin. J Endocrinol. 2007 Mar;192(3):605-14.

11. Ruderman NB, Xu XJ, Nelson LE, et al. AMPK and SIRT1: A longstanding partnership? Am J Physiol Endocrinol Metab. 2010 Apr;298(4):E751-60.

12. McGlothin P. Personal communication. May 25, 2010.

13. Picard F, Kurtev M, Chung N, et al. SIRT1 promotes fat mobilization in white adipocytes by repressing PPAR-gamma. Nature. 2004 Jun 17;429(6993):771-6.