Vicious Cycle – Aging and Declining Blood Sugar Control

Blog 18 – Age changes make it difficult to control blood sugar within a normal range.  Persistently high sugar levels create many problems.  The most significant is an acceleration of  aging that further promotes poor blood sugar control and hence high blood sugar

Hence, a vicious cycle is created that leads to preliminary stages of diabetes.  The origins of this cycle and effective means to disrupt it are presented in this blog and the next.

Introduction

Type 2 Diabetes (T2D) is the 7th leading cause of death in the elderly.  It is an insidious disease because there are no obvious early warning symptoms.  Moreover, T2D accelerates normal aging, increases the risk for heart disease and damages small blood vessels in multiple organs causing blindness, gangrene, reduced kidney function, impotence and neuropathy.  Fortunately, it is a potentially avoidable disease.

Prevention of T2D begins with assessment of fasting levels of blood sugar (clinically termed glucose).  A glucose concentration equal to or greater than 110 mg/100 ml of plasma after a 12-15 hour fast, obtained from repeat testing over 12 months, indicates an early but highly reversible stage of diabetes, termed prediabetes.  Other tests, HbA1c and glucose tolerance test (see Table 1 for details) are required to complement the fasting glucose values and could indicate progression to T2D.

Based on the most recent estimates by the CDC (2019), 26.4 million individuals over 65 have prediabetes based on results from one or more tests noted above.  However, this is an underestimation since many elderly avoid testing and thus remain uninformed on their risk for T2D.  

With a diagnosis of prediabetes, clinicians advise diet modification, weight loss and exercise (https://www.cdc.gov/diabetes/data/statistics-report/index.html).  While these strategies are effective if strictly followed, it is equally important for the elderly to understand the underlying reasons for the prediabetes in the first place and to have the option to minimize them.

The Influence of Aging on Blood Sugar Control

T2D is an age-related disease because aging influences blood sugar in two significant ways. 

    *One major age-related change is the well-documented decline in skeletal muscle mass. 

    *The second major change is the more recently documented age-related increase in the stress  hormone, cortisol.  Specifically, both resting and activated levels of cortisol increase with age and the response to stress is prolonged. 

Together, these age-allied modifications promote and sustain higher than normal levels of blood glucose, and thus create the prediabetic state.  Additionally, persistently high levels of glucose accelerate the deteriorative effects of aging, further disrupting glucose regulation.

Factor 1 – Age-Related Decline in Skeletal Muscle Mass

Several hormones and associated factors regulate blood glucose.  The most significant and most studied is insulin, a pancreatic hormone.  Following ingestion of food, metabolic processes liberate breakdown products such as glucose, amino acids and fatty acids into the blood.  Insulin, whose secretion is stimulated by rising glucose levels, facilitates the movement of these energy-rich nutrients especially glucose into the skeletal muscles for immediate use and into the fat and liver for storage. 

The problem for the elderly is this.  Skeletal muscle mass, comprising a significant portion (~40%) of total body mass, slowly declines with age.  It is the biggest consumer of available glucose whose delivery is assured by insulin.  However, if food consumption remains constant with age as it usually does, the same amount of glucose is still available BUT the end user e.g. the skeletal muscles, are reduced in size so less glucose is taken up.  Therefore, more glucose remains in the circulation and eventually is stored in the liver and fat.

The point is that with loss of muscle mass, circulating glucose remains higher for longer periods of time, supporting a prediabetic state.

Minimize Muscle Loss with Progressive Resistance Exercise

To keep blood glucose normal, muscle mass must remain constant.  Sadly, the loss of muscle mass with age is not obvious to most elderly.  This is because disappearing muscle tissue is replaced with fat deposits.  The only noticeable changes are a decline in muscle strength and associated unsteady balance.  A wealth of clinical trial data indicates that a program of progressive resistance exercise slows loss of muscle mass (and strength too).  It also improves insulin function called insulin sensitivity.  Insight 3, Progressive Resistance Exercise and Protein Supplements details these programs which may include free weights, resistance bands, weight machines and/or calisthenics.

An important corollary to a program of progressive resistance exercise is the recommendation to increase consumption of  proteins.  The building blocks of proteins are amino acids.  Amino acids stimulate muscle formation and are also incorporated into essential muscle proteins.  Quality proteins such as whey, soy and casein contain these amino acids. 

According to the government’s Recommended Daily Allowance (RDA), adults need to consume 56 grams of  protein each day to maintain general health.  In contrast, biogerontologists whose focus is the health span of the elderly, found the RDA to be inadequate for the elderly.  Consequently, the new, science-based recommendation for the elderly is twice the RDA.  To optimize muscle size and function, it is reasonable to consume quality proteins (whey, soy, casein containing essential amino acids) with meals and about 2 hours after a workout of resistance exercises.

Two Opposing Sides to Glucose

Glucose is an excellent source of energy for all cells in the body.  In contrast, it has a destructive side.  Glucose is a notorious oxidizer.  This means that glucose has the potential to  indiscriminately attack and damage nearby proteins, fats and DNA in tissues and cells.  Such oxidative modifications, if not repaired, contribute to reduced function and inflammation, hallmarks of aging.  Oxidative damage across the board makes it infinitely harder to keep glucose within an acceptable physiological range.

Vicious Cycle

Conclusions

It is incredibly important to maintain adequate control of  blood glucose.  In particular, glucose needs to be around long enough to provide a ready supply of energy to our muscles, but not long enough to exert oxidative damage.  Unfortunately, glucose is higher from longer periods of time in the elderly. This is because the muscles, the major consumer of glucose, diminish in size with age.  A program of progressive resistance exercise maintains muscle mass. However, absent this strategy, there is a risk of oxidative destruction to tissues and cells and a platform for prediabetes.

The second obstacle to  control of normal blood sugar is the age-related change in the stress response.  This is the topic of my next blog.

Table 1 – Tests Assessing Blood Sugar Control

TestMeasurementAbnormal Glucose Control  
Fasting GlucoseConcentration of glucose in the blood after
12-15 hour fast
Equal to or greater than
110 milligrams/100 ml
HbA1cOxidation (glycation) of hemoglobin Equal to or greater than 5.7%
Glucose Tolerance TestGlucose levels following ingestion of 1 gram sugar/kg body wt. Glucose peak >140 mg/100 ml;
4-6 hours to return to near baseline
Select References:

Duchowny K et al., Muscle Weakness and Physical Disability in Older Americans: Longitudinal Findings from the U.S. Health and Retirement Study. Nutr Health Aging.  22(4): 501–507, 2018.

Gomes MJ et al., Skeletal muscle aging: influence of oxidative stress and physical exercise. Oncotarget 8: 20428-20440, 2017.  

Paddon-Jones, Rasmussen BB. Dietary protein recommendations and the prevention of sarcopenia.  Curr Opin Clin Nutr Metab Care. 12(1):  86–90, 2009.

Yau JW, Thor SM, Ramadas A. Nutritional Strategies in Prediabetes: A Scoping Review of Recent Evidence. Nutrients  12:  2990, 2020.

Zand A, Ibrhim K, Patham B. Prediabetes: Why Should We Care?  Methodist Debakey Cardiovasc J. 14 (4):  289-297, 2018.