By Dr. Harry Pruess, M.D.

Over twenty years ago, way back in 1997, I wrote an editorial for a series of papers to appear in the Journal of the American College of Nutrition1.  My editorial focused on a potential, significant role for the glucose-insulin system in the aging process.  It was already recognized that the disorder in that metabolic schema known as diabetes was strongly associated with premature aging.  The question I raised then was whether mild dysfunctions of that particular system, short of diagnosed diabetes, could hasten the aging process over time. This concept is important because virtually everyone undergoes some dysfunction, even if mild, in this system over a lifespan. Importantly in many cases, it can be to some extent avoided2.

Although, I have touched upon some necessary background material in previous reports, additional information may still be necessary to understand where I’m coming from in offering this theory.

  1. In the 1920’s Banting and Best discovered insulin, a hormone that helped transport energy in the forms of glucose and free fatty acids into cells — particularly the cells  of muscle, fat, and liver. From this discovery, the theory arose that diabetes was simply a disorder of insulin lack and replacement would totally solve the malady. The latter situation does exist and is designated type 1.  However, it is not in this day and age the major form of diabetes mellitus.
  2. A decade later, some curious physicians reported a more common type of diabetes indicated of course by markedly elevated levels of blood glucose where the circulating levels of insulin were normal or even raised. This ubiquitous form of diabetes was labeled type 2 and was largely due to a poor peripheral organ response to insulin – “insulin resistance”3
  3. “Compensation” for this weaker reaction develops initially in an effective manner. The insulin producing cells of the pancreas put out more insulin than usual and raises its concentration to return the glucose at least partially toward normal. A back and forth of this situation continues as time passes resulting in a continual rise of both glucose and insulin.  The usual scenario is that as we grow older the elevation in both constituents usually stays in the designated normal range, but nevertheless in some unfortunate individuals insulin resistance takes its toll. The maximal insulin compensatory output is reached, the glucose levels continue to rise unabated, and diabetes develops. If the glucose–insulin levels only rise “mildly” but does not elevate to the level of diabetes, the question posed earlier is whether we would be better off if this slight increase never occurred1.  
  4. Insulin resistance is associated with type 2 diabetes as mentioned above, obesity, disturbances in circulating lipids such as triglycerides and HDL-cholesterol, elevated blood pressure, fatty liver, and general inflammation – all chronic condition associated with aging and characteristically referred to as the “metabolic syndrome4.” Most experts believe that insulin resistance goes beyond just being “an associate” and is actually the driving force behind the elements of the metabolic syndrome5.
  5. Important in all this, excellent safe natural  means to slow progress or even essentially prevent insulin resistance are available2.

Hopefully, the reader has understood the reasoning behind the concept concerning a potential significant role of mild insulin resistance in the aging process.  Still, can we strengthen this concept? In the case of examining useful, healthful lifespan, the public as a whole will not follow any regimen to institute the scenario described above unless more definitive proof is put before them.  

Logic dictates that studies regarding lifespan are difficult to develop and carry out.  Why? Simply because subjects may outlive the investigator. Therefore, markers for aging are often substituted for actual direct proof of increased longevity, but this is usually not enough.  We have too many doubting Thomases to expect widespread acceptance otherwise. Despite all of this, I believe there does exist plausible evidence to implicate mild forms of insulin resistance in the aging process – enough sound substantiation to undertake an anti-aging regimen that keeps insulin resistance as weak as possible – even throughout early life!  Detailing the “aging paradox” and specific animal studies will be the objective of the next report.

References

  1. Preuss HG:  The insulin system in health and disease.  J Amer Collu Nutr 16:393-394, 1997.
  2. Preuss HG, Clouatre D: Potential of diet and dietary supplementation to ameliorate the chronic clinical perturbations of the Metabolic Syndrome. In: Nutritional and Integrative Strategies in Cardiovascular Medicine. (eds) S Sinatra and M Houston, CRC Press, Boca Raton Florida, pp 148-178, 2015. 
  3. Reaven GM: Banting lecture 1988. Role of insulin resistance in human disease. Diabetes 37:1595-1607
  4. DeFronzo RA, Ferrannini E: Insulin resistance. A multifaceted syndrome responsible for NIDDM, obesity, hypertension, dyslipidemia, and atherosclerotic cardiovascular disease.  Diabetes Care 14:173-194, 1991.
  5. Reaven GM: The individual components of the metabolic syndrome: Is there a raison d’etre?  J Amer Coll Nutr 6:191-195, 2007.  

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