Another important and more recent biomarker for health is based on hemoglobin A1c, which is a form of hemoglobin that measures the average plasma glucose concentration over a six to twelve week period. [Note: This post is a bit more technical than normal!]
Average plasma glucose varies based on the amount of glycation, where a protein molecule bonds to a sugar molecule WITHOUT the controlling action of an enzyme. This is a haphazard situation, because without the controlling enzyme, it causes damaged and abnormal tissues, as well as resulting health implications that develop.
On the other hand, glycosylation, an enzymatic process where a carbohydrate is added to a protein or fat WITH the controlling action of an enzyme, is ideal for optimum health. This controlling enzyme signals the function of cell changes and appropriate use of sugar, which gives proteins or fats the ability to control many healthy cell functions.
Normally, HbA1c has been associated as an important biomarker for diabetes, but really, it is a measurement of the ratio of these two latter reactions; glycosylation vs. glycation. Indeed, HbA1c accurately assesses the ratio between these two important processes, which paints a greater picture of chronic damage in the body.
The optimum range of HbA1c is between 4.5% and 5.5%, and anything above that indicates damage. If this is the case, you should have your levels measured every three months, because just as mold creeps up on a house, glycation creeps up in our cells. This can cause illnesses that affect ALL body systems like cardiovascular disease, retinal dysfunction, diabetes, and neurological disease like Alzheimer’s.
In fact, I have uncovered studies dating back to 1994 linking HbA1c levels to Alzheimer’s disease (Yan, et. al, 1994). This frightening disease affects over 5 million Americans today and is expected to triple by 2050, and modern science is treating this epidemic like it’s a big mystery (Alzheimer's Association, 2013).
Folks, it’s not a mystery! The cause is a brain on fire from either sugar disregulation in the body, or stemming from an inflammatory process starting in the gut. Because the gut and the brain are connected via the gut-brain axis, inflammation in the gut causes inflammation in the brain.
So, how can we positively affect
glycosylation, or how sugar is effectively processed in the body?
1) Performing Short, High Intensity Intervals Exercising with high intensity intervals three times per week has been shown to improve glycosylation (Casteneda, 2002). This is even without diet changes! For interval training ideas, check out my post
here.
2) Consuming More Healthy Fats and Less Carbohydrates
Other studies show the beneficial effects of a ketogenic-like diet, which involves consuming more healthy fats and less carbohydrates (Hussain, et. al., 2012). Bring on the greens, eggs, avocados, and olive oil!
3) Heal the Gut to Heal the BrainHealing the gut aids in healing inflammation in the brain. For ways to do so, read my post
here.
4) Decrease Overall Inflammation
Beyond healing the gut, decreasing overall inflammation by managing stress, getting an appropriate amount of sleep, and consuming a wide variety of colorful vegetables are all helpful in decreasing fire in the body!
References
Alzheimer's Facts and Figures. (2013). Alzheimer's Association. http://www.alz.org/alzheimers_disease_facts_and_figures.asp.
Casteneda, C, Layne, J, Munoz-Orians, L, Gordon, P, Walsmith, J, Foldvari, M, Roubenoff, R, Tucker, K, and Miriam Nelson. (2002). A randomized controlled trial of resistance exercise training to improve glycemic control in older adults with type 2 diabetes.
American Diabetes Association. http://care.diabetesjournals.org/content/25/12/2335.long.
Hussain, TA, Mathew, TC, Dashti, AA, Asfar, S, Al-Zaid N, Dashti, HM. Effect of low-calorie versus low-carbohydrate ketogenic diet in type 2 diabetes.
Nutrition.
http://www.ncbi.nlm.nih.gov/pubmed/22673594.
Yan, SD, Chen, X, Schmidt, AM Brett, J, Godman, G, Zou, YS, Scott, CW, Caputo, C, Frappier, T & MA Smith. (1994). Glycated tau protein in Alzheimer disease: A mechanism for induction of oxidant stress.
National Academy of Sciences of the United States of America. Vol. 91, no. 16: 7787-7791.
http://www.pnas.org/content/91/16/7787.abstract.