Do you know what a normal blood sugar reading is? Better yet, do you know what your blood sugar reading is? If you do, that’s great. However, you should know that the established criterion for normal fasting glucose (up to 100 mg/dL) has been outdated for quite some time. Fasting glucose should be less than 86 mg/dL. Studies show that excess glucose damages your body, long before a diagnosis of either prediabetes or diabetes is established.
Glucose crosses the digestive lining, moves into the bloodstream, and enters cells, where it is used as energy. Alpha glucosidase, an enzyme in the intestines, transports glucose from the gut and into the bloodstream. Insulin is the hormone that takes up glucose into cells. Insulin, however, does more than regulate blood glucose levels. It is also involved in stimulating cell growth and differentiation.
Excess Glucose is Sticky Business
Unfortunately, the Western diet is made up of carbohydrate-rich foods that produce an excess amount of glucose after meals. Sugar spikes after meals result in excess sugars stored as fat, which may cause weight gain. Extra glucose circulating in the bloodstream also damages endothelial cells, which make up the inner wall of blood vessels. The sticky glucose molecules promote inflammation within the arteries; over time, the damage caused by excess glucose may develop into vascular disease, affecting heart and brain health.
In integrative medicine, practitioners recognize that excess glucose increases the risk for many chronic diseases other than type 2 diabetes (such as cardiovascular disease, dementia, and cancer). Since glucose is a modifiable risk factor, it is imperative that experts begin to recognize that a fasting glucose level below 86 mg/dL is optimal for good health.
To underscore the importance of maintaining healthy blood glucose levels, studies show that excess glucose destroys the structural integrity of arteries, which results in coronary and cerebral vascular diseases.1 When it comes to brain health, extra circulating sugars can interrupt normal brain function, even at high-normal glucose levels. The amygdala and hippocampus (brain areas that are critical to memory) were noted to undergo atrophy when they were chronically exposed to high-normal blood sugar levels, which led to memory deficits.2 Numerous studies have also linked excess glucose to an increased risk of cancer.3-5
Data are robust in showing that post-meal sugar spikes are detrimental to your health. Your risk of cardiovascular death is the greatest within the first two hours after you’ve had a meal.6 That’s because post-meal sugar spikes can immediately impede blood flow through vital arteries, which can ultimately lead to a heart attack or stroke.7
Maintain Healthy Blood Sugar Levels
- Avoid refined carbohydrates and processed foods: White flour, white sugar, white bread, desserts, pastries, bagels, and more are high in sugar and have little to no nutritional value. These foods tend to be high in salt, sugar, and calories.
- Eat five or more servings of fruits and vegetables daily: Grapes, berries, apples, grapefruit, tomatoes, broccoli, Brussels sprouts, and carrots contain various nutrients, vitamins, minerals, and antioxidants that provide energy and protection to the body.
- Add fiber to your diet: Fruits, nuts, seeds, legumes, and whole grains contain loads of fiber. Fiber helps to keep you fuller longer (when people experience a hunger spell, they tend to snack on starchy foods that don’t contain much or any fiber, which leads to excess sugar in the bloodstream).
- Supplement your diet: There are pharmaceutical-grade supplements that function similarly to drugs that are used to regulate type 2 diabetes. Mulberry leaf extract lowers glucose by enhancing the activity of GLUT4, the energy transporter that moves glucose from the bloodstream into cells.8 Similar to metformin, a drug used to treat type 2 diabetes, mulberries also block excess gluconeogenesis (the production of glucose by the liver during fasting).9,10 Alternatively, you can eat dried mulberries, too. Although dried fruits tend to contain lots of sugar, this is not the case for dried mulberries. Mulberries are also loaded with antioxidants, fiber, and protein. Another supplement is phloridzin, and it blocks a glucose transport system in the gut to prevent post-meal sugar spikes.
Ma S, Virkama A, Groop P-H, et al. Chronic hyperglycemia impairs endothelial function and insulin sensitivity via different mechanisms in insulin-dependent diabetes mellitus. Circulation. 1996;94(6):1276-1282.
Cherbuin N, Sachdev P, Anstey KJ. Higher normal fasting plasma glucose is associated with hippocampal atrophy The PATH Study. Neurology. 2012;79(10):1019-1026.
Larsson SC, Mantzoros CS, Wolk A. Diabetes mellitus and risk of breast cancer: A meta‐analysis. International journal of cancer. 2007;121(4):856-862.
Xue F, Michels KB. Diabetes, metabolic syndrome, and breast cancer: a review of the current evidence. The American journal of clinical nutrition. 2007;86(3):823S-835S.
5. Alokail MS, Al-Daghri NM, Al-Attas OS, Hussain T. Combined effects of obesity and type 2 diabetes contribute to increased breast cancer risk in premenopausal women. Cardiovasc Diabetol. 2009;8(1):33.
Lin H-J, Lee B-C, Ho Y-L, et al. Postprandial glucose improves the risk prediction of cardiovascular death beyond the metabolic syndrome in the nondiabetic population. Diabetes Care. 2009;32(9):1721-1726.
Nitenberg A, Cosson E, Pham I. Postprandial endothelial dysfunction: role of glucose, lipids and insulin. Diabetes & metabolism. 2006;32:2S28-22S33.
Carvajal R, Rosas C, Kohan K, et al. Metformin augments the levels of molecules that regulate the expression of the insulin-dependent glucose transporter GLUT4 in the endometria of hyperinsulinemic PCOS patients. Human Reproduction. 2013;28(8):2235-2244.
Andallu B, Varadacharyulu N. Gluconeogenic substrates and hepatic gluconeogenic enzymes in streptozotocin-diabetic rats: effect of mulberry (Morus indica L.) leaves. Journal of medicinal food. 2007;10(1):41-48.
Kim YD, Park K-G, Lee Y-S, et al. Metformin inhibits hepatic gluconeogenesis through AMP-activated protein kinase–dependent regulation of the orphan nuclear receptor SHP. Diabetes. 2008;57(2):306-314.