Old Nutrient, New Application
NUTRITION
BT Watts
As far back as the late nineteenth century, the health science establishment began looking into GABA as a metabolic product derived from plants and microbes. Not too many applications for people, but “nice to know” in the world of botany. Fast forward a few decades to the 1950s and GABA breaks onto the health science stage, identified as an integral part of nervous system activity, mainly acting as the primary inhibitory neurotransmitter.
GAB Anergic activity is now being harnessed and controlled to help a variety of patients who suffer from a variety of health conditions. GABA, by all accounts, has been an important discovery for health science, so much that you often can find GABA in supplement form on the shelves of your local supermarket. GABA in supplement form purportedly has a variety of uses related to health and wellness.
Interestingly, it appeals that GABA may perform and have application for about 29 million Americans who suffer from type 2 diabetes. As most practitioners are aware, the CDC reports that roughly 29 million people suffer from type 2 diabetes. Likewise, most practitioners are aware that results for type 2 diabetics are often quite poor.
Emerging clinical literature appears to show promise for patients suffering from type 2 diabetes, as it relates to GABA supplementation. It appeal s that the careful application and timing of GABA as a dietary supplement has been shown to support the body’s ability to suppress glucagon activity. In particular, the supportive nature of GABA appears to suppress postprandial
elevations of glucagon in response to insulin resistance. GABA has also been shown to support proper beta cell function, thereby potentially increasing the effectiveness of the body’s insulin response in a hyperglycemic state.
A paradigm shift in the functional health community appeal s to be needed, relative to how we think about and understand insulin resistance in order to explore the benefits of GABA for the dysglycemic patient population. The current clinical literature has demonstrated that even postprandial glucagon can increase, which in turn can cause and increase in serum blood sugar. Further, the increase in postprandial glucagon appears to promote insulin resistance among the alpha cells of the pancreas. The net effect of this mechanism appeals to be increased insulin resistance, increased blood sugar, and overall poor control of the diabetic condition. The emerging understanding of this particular mechanism could be a game changer relative to how we support our type 2 diabetic patients.
As previously stated, GABA has been shown to be useful in supporting the body’s ability to dampen or blunt the postprandial release of glucagon. However, it is quite interesting that postprandial glucagon secretion is almost never discussed in terms of a primary mechanism for elevated blood glucose in the type 2 diabetic population. The strategic application of GABA as a dietary supplement in a clinical setting to the type 2 diabetic population is showing promise. Finally, the supportive application of GABA is a unique way to separate and distinguish oneself from other healthcare providers.
Following you will find some excerpts from research papers
that speak to the effects of GABA in an experimental setting. In some instances, I have provided my own clinical opinion regarding the excerpt.
"Gamma aminobutyric acid (GABA) exerts P-cell regenerative and immunoregulatory effects. Specifically, GABA stimulates P-cell replication, protects P-cells against apoptosis, and attenuates insulitis. These effects result hi an enhanced functional P-cell mass and, in mice, this can reverse disease...” It is my opinion that the beta cell replication possibility alone warrants the consideration of using GABA hi a clinical model where type 2 diabetes is being supported.
And then, in a study organizing patients with type 2 diabetes, GABA was added to their existing treatment model. “GABA significantly increased circulating insulin levels in the subjects under either fasting or fed conditions. GABA also increased glucagon levels only under fasting conditions.”
This seems to mean that the effect of GABA on the pancreas was observed, both during fasting and fed conditions, all while still blunting glucagon levels in the postprandial state. The selective nature of the “GABA effect” on hyperglycemia has also been encouraging in a clinical setting.
The researchers went on to say, “Importantly, GABA significantly decreased glycated albumin levels in the repeated dosing period.”
The use of GABA should be in strong consideration for those diagnosed with either prediabetes or full-fledged type 2 diabetes. This consideration should be even stronger with patients who apparently are not producing enough endogenous insulin.
The volume of GABA required for the documented clinical results in the aforementioned studies is a whopping 2 grams. Even if you could dose 2 grams of GABA in a single dose to your patients, the likelihood of an acceptable absoiption rate in products off the shelf is not strong. Ifyou are considering using GABA with your patients, it’s my opinion that liquefied GABA held in a liposomal suspension offers the greatest opportunity for adequate and efficient bioavailability.
In summary, GABA has the potential to support those suffering the challenges of hyperglycemia in a way few nutrients can. While GABA has been shown to have beneficial effects on the central nervous system, its action at the endocrine level may hold the most curious and promising application—selective dampening of glucagon while upregulating the insulin response. When considering the clinical action of GABA for your
patient base, be selective with your mode of delivery and opt for an absorption-increasing mechanism such as oral liposomal technology.
References:
1. CellMetab. 2006 Jan;3(l):47-58. Intra-islet insulin suppresses glucagon release via GABA-GABAAreceptor system. Xu E1, Kumar M, Zhang Y, Ju W, Obata T, Zhang N, Liu S, Wendt A, Deng S, Ebina Y, Wheeler MB, Braun M, Wang Q.
2. Front Pharmacol. 2015 Nov 10;6:260. doi: 10.3389/ fphar.2015.00260. eCollection 2015. Study of GABA in Healthy Volunteers: Pharmacokinetics and Pharmacodynamics. Li J1, Zhang Zl, Liu XI, Wang Yl, Mao FI, Mao J2, Lu XI, Jiang Dl, Wan Yl, Lv JY3, Cao G4, Zhang J4, Zhao N3, Atkinson M5, Greiner DL6, Prud’homme GJ7, Jiao Z2, Li Yl, Wang Q8.
3. Diabetes. 2014Dec;63(12):4197-205. doi: 10.2337/db 14-0153. Epub 2014 Jul 9. GABA promotes human P-cell proliferation and modulatesglucose homeostasis. Purwana II, Zheng Jl, Li Xl,DeurlooM2, Son DOI, ZhangZ3, Liang Cl, ShenEl,Tadkase A4, Feng ZP2, Li Y3, Hasilo C5, Paraskevas S5, Bortell R6, Greiner DL6, Atkinson M7, Prud’homme GJ8, Wang Q9.
Dr. Watts is a highly respected and experienced leader in the space of health and wellness and in particular Functional Medicine & Clinical Nutrition. He has extensive experience in clinical practice having reviewed and analyzed more than 15,000 lab panels. He is the owner of 2 successful functional medicine clinics and has been instrumental in helping thousands of chronically illpatients return to health. Dr. Watts is also a very accomplished trainer of other clinicians in the area of laboratory analysis andpatient care. For more information on this and other products visit www .biogerretix.com or call us at 720-287-2155.
