Over the last several weeks we’ve talked about several topics related to leaky gut, autoimmunity and gluten sensitivity. This week we’re going to shift gears a bit and cover how to keep blood sugar stable. More specifically, this article will focus on treatments for reactive hypoglycemia (RH), which is a type of blood sugar dysregulation.

Functional medicine considers RH to be a lifestyle disorder that results from the overconsumption of refined carbohydrates and sugar and is a form of “post prandial hypoglycemia,” which means that the hypoglycemia occurs after eating a meal. In Western medicine, true reactive hypoglycemia is considered to be relatively rare and is often referred to as “idiopathic post prandial hypoglycemia,” or reactive hypoglycemia with an unknown cause.

But even research which expresses skepticism about the prevalence of RH will often observe that people with RH “are characterized as ingesting excessive quantities of refined carbohydrate.” This same study goes on to conclude that one critical arm of treatment is the restriction of refined carbohydrates, which would also include sugar (1).

Consequences of reactive hypoglycemia

I often describe RH as “a blood sugar rollercoaster.” Blood sugar dysregulation and reactive hypoglycemia have been associated with an increased risk of many diseases, including diabetes as well as heart disease and Alzheimer’s disease. Some research is beginning to show that highly variable blood sugar may be more damaging to the body than chronic hyperglycemia.

Reactive hypoglycemia is also often implicated in mood and anxiety disorders like depression and bipolar disorder in particular. A blood sugar rollercoaster does not promote a stable mood. In contrast, stable blood sugar helps maintain a stable mood and even temperament. RH has also been implicated as a significant causative factor for violence and aggression in the prison population.

Perhaps most striking is the link between RH and metabolic disease in general and Type 2 diabetes in particular. According to the 2014 Statistics Report published by the CDC, 21 million Americans, or 9.3% of the United States population have Type 2 diabetes(2).

HPA axis dysregulation

Another possible consequence of reactive hypoglycemia is problems with the hypothalamus – pituitary – adrenal axis. When blood sugar crashes and a person becomes hypoglyemic, the adrenal glands are stimulated and release cortisol. Cortisol a stress hormone that raises blood sugar through a process call gluconeogenesis.

Various causes can lead to HPA dysregulation and adrenal hypofunction, which can in turn result in chronically low levels of cortisol. Long-standing reactive hypoglycemia can be a primary cause of functionally depressed cortisol, as the adrenal glands are frequently stimulated in order to raise blood sugar. Over time, this increased demand on the adrenals can lead to chronically depressed cortisol levels.

Functionally low cortisol, also known as hypocorticolism, can result in a decreased ability to handle blood sugar dips. A person who easily becomes hypoglycemic when a meal is missed may have functional hypocorticolism. Chief signs and symptoms include low blood sugar, low blood pressure, frequent urination and fatigue. This indicates HPA downregulation. Reactive hypoglycemia can lead to a vicious cycle of hypoglycemia that the adrenals are unable to handle.

Functional hypocorticolism can be tested for by performing a DUTCH adrenal dried urine lab test, which evaluates cortisol levels four times over the course of a 24 hour period. This type of testing, performed by a functional medicine practitioner, can reveal whether HPA downregulation is at the root of hypoglycemia symptoms.

Causes of reactive hypoglycemia

RH is a lifestyle disorder that primarily results from overconsumption of refined carbohydrates and sugar in the absence of sufficient protein and fat, but carbohydrates are not the only cause. Other factors can influence blood sugar and contribute to RH as well, such as H. pylori infection of the stomach mucosa. A third cause of reactive hypoglycemia can be toxic metal poisoning.

Overconsumption of refined carbohydrates and sugar

When we consume a well-balanced meal of moderate carbohydrate, adequate protein and plenty of healthy fats, blood sugar is maintained within a fairly narrow range. After eating, blood sugar rises and gradually declines over the course of several hours, due to the effects of insulin. This anabolic hormone prompts the body to carry circulating glucose out of the bloodstream and into cells to be burned for energy. After a meal, a modest increase in blood sugar gradually returns to baseline several hours later, at which point we would eat another meal.

In contrast, a reactive hypoglycemia diet is characterized by excessive consumption of refined carbohydrates and sugar, often in the absence of sufficient protein and fat. Refined carbohydrates and sugar cause a spike in blood sugar, which quickly rises to dangerous levels. In response to soaring blood glucose levels, the pancreas releases large amounts of insulin in an attempt to bring blood sugar back down.

In reactive hypoglycemia, the amount of insulin secreted by the pancreas exceeds the amount needed to control blood sugar and hyperglycemia gives way to hypoglycemia, or low blood sugar. This typically happens 1-3 hours after a meal and results in characteristic hypoglycemia symptoms of shaking, sweating, feeling cold, dizziness, and difficulty thinking. It can also lead to irritable and even aggressive behavior, or what many people commonly refer to as being “hangry.”

H. pylori

Helicobacter pylori is a gram-negative bacterium that infects the stomach and sometimes the upper small intestine. Due to its unique spiral shape, H. pylori can burrow into the mucus lining the stomach where it is protected from the harsh acidic environment of the stomach.

H. pylori increases the secretion of gastrin, a key digestion hormone that in turn stimulates the release of insulin. As a result, higher levels of insulin are secreted after meals, resulting in hypoglycemia symptoms. For this reason H. pylori appears to contribute to RH in some people (3) (4).

Worldwide, H. pylori is a very common infection. Scientists estimate that half of the world’s population is infected (5), but that number appears to be much lower in the United States. One large review of biopsies found a prevalence of 7.5% in the US (6). Your functional medicine practitioner can order an H. pylori breath test if s/he suspects H. pylori may be present.

Toxic metal poisoning & trace mineral deficiency

A number of toxic metals, commonly referred to as “heavy metals,” have been implicated in reactive hypoglycemia. Another potential cause that can occur either in combination with, or independent of toxic metal accumulation, is deficiency of several trace minerals.

Toxic metals are described in research as being “hyperglycemic,” or leading to elevated blood sugar, whereas several nutritive trace minerals enhance the effects of insulin and lower blood sugar. These metals are “hypoglycemic” and have demonstrated positive clinical applications for metabolic disease.

Hyperglycemic toxic metals include arsenic, mercury, iron, lead, nickel and cadmium. Your functional medicine practitioner can test for toxic metal accumulation in the body and help you reduce this toxic burden if necessary.

Hypoglycemic minerals include zinc, vanadium, chromium and magnesium. These minerals can be toxic or nutritive, depending on the dose. In many cases, both depressed and elevated levels of these minerals have negative effects.

Zinc is required by the pancreatic beta cells for insulin secretion, synthesis and storage. Deficiency of zinc is associated with both hyperglycemia and diabetes (7). However, there can be negative consequences of elevated zinc levels as well. A rat study showed that metabolic syndrome was promoted by long term zinc supplementation (8).

Vanadium enhances the effects of insulin by inhibiting tyrosine protein phosphatases, which upregulates phosphorylation of various insulin pathway intermediaries (9). On the other hand, acute vanadium intoxication can lead to life-threatening hypoglycemia (10).

Chromium lowers blood sugar by promoting glucose catabolism in muscle cells and lipocytes (fat cells) (11). Chromium also increases insulin sensitivity and reduces inflammatory markers TNF-alpha, resistin and interleuken-6 (12). Of the three, chromium apperas to be the most safe and chromium toxicity appears to be rare.

Magnesium is unequivocally an essential nutrient. It is a cofactor for carbohydrate metabolism through its role in ATP-dependant enzymatic reactions. In addition, magnesium deficiency is associated with insulin resistance and Type 2 diabetes (13).

Treatments for reactive hypoglycemia

The most important component of addressing reactive hypoglycemia is the diet. No magic combination of supplements or exercise can compensate for a diet that is too high in refined carbohydrates and sugar. The unavoidable first step in stabilizing blood sugar involves making dietary changes. Keep reading for more detailed information on how to eat to avoid RH.

Key points of the RH diet:

• Include adequate protein in the diet from organic, pasture-raised beef, lamb, and chicken; wild-caught cold-water fish like salmon and sardines; and pseudo-grains like quinoa.
  • Make sure every meal and snack has some protein
• Include adequate healthy fats like unrefined coconut oil, avocado, cold-pressed olive oil and ghee.
  • Fats provide stable energy that is metabolized more slowly than carbohydrates, which promotes more stable blood sugar.
  • Avoid unhealthy fats such as vegetable oils, inluding soybean, safflower, corn, and Canola. Also avoid fried foods.
• Avoid refined carbohydrates, sugar and artificial sweeteners
  • Focus on starchy vegetables like carrot, parsnip, sweet potato, taro and yucca root.
  • Reduce sugar and try stevia-sweetened alternatives like Lily’s chocolate
• Eat regularly to keep blood sugar stable and don’t skip meals!
  • Pay attention to feelings of hunger and give your body what it needs to function properly.
  • Eat a snack every 2-3 hours at first, then space back meals back out as blood sugar stabilizes.
  • Consume healthy fats before bed. Drink 1-3 tsp coconut oil in a cup of chamommile tea before bed

Nutrients & Botanicals

Vitamin C and Vitamin E, when combined with chromium were shown to improve fasting glucose, HgA1C and insulin sensitivity (11).

Chromium itself has been shown to reduce elevated blood sugar levels but caution should be exercised with all hypoglycemic nutrients not to push blood sugar too low.

Magnesium is a commonly deficient nutrient and low levels have consistently been found in people with elevated insulin (14) (15) (16).

Cinnamon can help lower blood sugar levels and has also been shown to lower triglycerides, LDL cholesterol and total cholesterol (17).

Berberine is an herb commonly used for its anti-inflammatory and anti-diabetic properties. In addition to lowering blood sugar, berberine improves triglyerides, HbA1C fasting insulin and total cholesterol (18). The hypoglycemic effects of berberine are well established and may be useful in RH as well. The mechanism of action for berberine is not fully understood but one primary component appears to be stimulation of the GLUT4 receptor. Glucose transporter 4, or GLUT4 shuttles glucose out of the blood stream and into skeletal muscle, thereby lowering blood sugar.

Gynostemma is another herb with hypoglyemic properties. Although not as well researched as berberine, gynostemma has shown benefit in Type 2 diabetes (19) and may be also useful in regulating blood sugar in RH. Gynostemma appears to work by inhibiting the PTP1B enzyme. Levels of PTP1B are inversely correlated with insulin sensitivity and obesity in mice (20).

Blood sugar *balance*

It’s important to remember that a primary mechanism of action for many of these nutraceuticals is lowering blood sugar. In cases of elevated blood sugar, this would be desirable. But if used improperly when blood sugar is already too low, they may add insult to injury by lowering blood sugar even further. Blood sugar is a balancing act and your functional medicine practitioner can help you determine the best course of action.

It’s difficult to provide specific supplement advice for reactive hypoglycemia that will help everyone because each case is different. That being said, these nutraceuticals are probably best used to control and prevent hyperglycemic blood sugar spikes that trigger the massive insulin response associated with RH. Regulating blood sugar while addressing other areas like diet, H. pylori and other related issues can help a person to feel better sooner and make the transition towards stable blood sugar a bit faster and easier.

Other treatment options

Testing: If you find that eating a more RH-friendly diet doesn’t improve your symptoms, consider delving deeper into other causes like H. pylori with testing from your functional medicine practitioner. Another important testing option is DUTCH adrenal dried urine testing, which can confirm or rule out HPA axis downregulation. This test, which was mentioned earlier in the HPA Axis Dysregulation section, can provide valuable information to illuminate the root cause behind reactive hypoglycemia.

Mind root cause: If you struggle to reduce sugar and refined carbohydrates it can also be valuable to spend some time reflecting on what role these substances fill in your life. Are there unexpressed feelings or unresolved conflict underlying this struggle? Are sweet or starchy indulgences a way to manage loneliness or boredom? Approach these questions from a non-judgmental place of compassionate curiosity. Strive to explore and understand your cravings. They will likely reveal clues that will help you resolve your cravings on a deeper level than resorting to will power alone will.

Sleep: Good quality sleep, and the right amount of it, is crucial (21).

References

1. Hofeldt, Fred D. “Reactive Hypoglycemia.” Metabolism 24.10 (1975): 1193-208. Web.
2. “2014 National Diabetes Statistics Report.” Centers for Disease Control and Prevention. Centers for Disease Control and Prevention, 15 May 2015. Web. 12 May 2017.
3. Açbay, Özer, Aykut Ferhat Çelik, and Sadi Gündoğdu. “DoesHelicobacter Pylori-induced Gastritis Enhance Food-stimulated Insulin Release?” Digestive Diseases and Sciences41.7 (1996): 1327-331. Web.
4. Açbay, Ö., P. Kadioglu, A. Celik, and S. Gündogdu. “Helicobacter Pylori-induced Gastritis May Contribute to the Occurrence of Postprandial Symptomatic Hypoglycemia.” Gastroenterology 114 (1998): n. pag. Web.
5. Brown, L. M. “Helicobacter Pylori: Epidemiology and Routes of Transmission.” Epidemiologic Reviews 22.2 (2000): 283-97. Web.
6. Sonnenberg, Amnon, Richard H. Lash, and Robert M. Genta. “A National Study of Helicobactor Pylori Infection in Gastric Biopsy Specimens.” Gastroenterology 139.6 (2010): n. pag. Web.
7. Capdor, Jasmine, Meika Foster, Peter Petocz, and Samir Samman. “Zinc and Glycemic Control: A Meta-analysis of Randomised Placebo Controlled Supplementation Trials in Humans.” Journal of Trace Elements in Medicine and Biology 27.2 (2013): 137-42. Web.
8. Singh, Kshetrimayum Birla. “Long Term Excessive Zn Supplementation Induced Oxidative Stress in Wistar Rats Fed on Semi-Synthetic Diet.” Food and Nutrition Sciences 03.06 (2012): 724-31. Web.
9. Niu, Xia, Ruyue Xiao, Na Wang, Ziwei Wang, Yue Zhang, Qing Xia, and Xiaoda Yang. “The Molecular Mechanisms and Rational Design of Anti-Diabetic Vanadium Compounds.” Current Topics in Medicinal Chemistry 16.8 (2015): 811-22. Web.
10. Boulassel, Brahim, Nouredine Sadeg, Olivier Roussel, Martine Perrin, and Hafid Belhadj-Tahar. “Fatal Poisoning by Vanadium.” Forensic Science International 206.1-3 (2011): n. pag. Web.
11. Lai, Ming-Hoang. “Antioxidant Effects and Insulin Resistance Improvement of Chromium Combined with Vitamin C and E Supplementation for Type 2 Diabetes Mellitus.” Journal of Clinical Biochemistry and Nutrition 43.3 (2008): 191-98. Web.
12. Jain, Sushil K., and Krishnaswamy Kannan. “Chromium Chloride Inhibits Oxidative Stress and TNF-α Secretion Caused by Exposure to High Glucose in Cultured U937 Monocytes.” Biochemical and Biophysical Research Communications 289.3 (2001): 687-91. Web.
13. Garg, Neetika, Janice Weinberg, Sandeep Ghai, Gitana Bradauskaite, Matthew Nuhn, Amitabh Gautam, Nilay Kumar, Jean Francis, and Joline L. T. Chen. “Lower Magnesium Level Associated with New-onset Diabetes and Pre-diabetes after Kidney Transplantation.” Journal of Nephrology 27.3 (2014): 339-44. Web.
14. Wang, Jinsong, Gioia Persuitte, Barbara Olendzki, Nicole Wedick, Zhiying Zhang, Philip Merriam, Hua Fang, James Carmody, Gin-Fei Olendzki, and Yunsheng Ma. “Dietary Magnesium Intake Improves Insulin Resistance among Non-Diabetic Individuals with Metabolic Syndrome Participating in a Dietary Trial.” Nutrients 5.10 (2013): 3910-919. Web.
15. Hata, A., Y. Doi, T. Ninomiya, N. Mukai, Y. Hirakawa, J. Hata, M. Ozawa, K. Uchida, T. Shirota, T. Kitazono, and Y. Kiyohara. “Magnesium Intake Decreases Type 2 Diabetes Risk through the Improvement of Insulin Resistance and Inflammation: The Hisayama Study.” Diabetic Medicine 30.12 (2013): 1487-494. Web.
16. Rumawas, Marcella E., Nicola M. Mckeown, Gail Rogers, James B. Meigs, Peter W.f. Wilson, and Paul F. Jacques. “Magnesium Intake Is Related to Improved Insulin Homeostasis in the Framingham Offspring Cohort.” Journal of the American College of Nutrition 25.6 (2006): 486-92. Web.
17. Khan, A., M. Safdar, M. M. Ali Khan, K. N. Khattak, and R. A. Anderson. “Cinnamon Improves Glucose and Lipids of People With Type 2 Diabetes.” Diabetes Care 26.12 (2003): 3215-218. Web.
18. Zhang, Yifei, Xiaoying Li, Dajin Zou, Wei Liu, Jialin Yang, Na Zhu, Li Huo, Miao Wang, Jie Hong, Peihong Wu, Guoguang Ren, and Guang Ning. “Treatment of Type 2 Diabetes and Dyslipidemia with the Natural Plant Alkaloid Berberine.” The Journal of Clinical Endocrinology & Metabolism 93.7 (2008): 2559-565. Web.
19. Huyen, V. T. T., D. V. Phan, P. Thang, N. K. Hoa, and C. G. Östenson. “Antidiabetic Effect OfGynostemma PentaphyllumTea in Randomly Assigned Type 2 Diabetic Patients.” Hormone and Metabolic Research 42.05 (2010): 353-57. Web.
20. Elchebly, M. “Increased Insulin Sensitivity and Obesity Resistance in Mice Lacking the Protein Tyrosine Phosphatase-1B Gene.” Science 283.5407 (1999): 1544-548. Web.
21. Broussard, Josiane L., David A. Ehrmann, Eve Van Cauter, Esra Tasali, and Matthew J. Brady. “Impaired Insulin Signaling in Human Adipocytes After Experimental Sleep Restriction.” Annals of Internal Medicine 157.8 (2012): 549. Web.