DEMYSTIFYING
DETOXIFICATION

The word "detoxification" can trigger negative responses. When we think "detox," we think discomfort or fear. Patients wonder, "Will I be starving?" or "Will I be in the bathroom all day?" Detox, unfortunately, can be a scary prospect for patients.

Truth be told, our bodies naturally detox every day. Detoxification enables us to discard foreign, unwanted, non-nutritive, or chemical substances that enter our food supply, poison our lakes and rivers, and find their way into cookware and clothing. Some toxins are even produced by our own metabolic processes.

Because toxin buildup is linked to chronic health issues like cardiovascular disease, diabetes, autoimmune disease, neurological diseases, reproductive disease, ADD/ADHD/autism, depression, and anxiety, it is important that we communicate our natural detoxification ability to patients.

Detox happens in two phases: phase I and phase II, converting fat-soluble toxins into water-soluble compounds for excretion. In phase I, cytochrome P450 enzymes (CYPs) in the liver and intestines transform toxins into a water-soluble form, metabolized by phase II enzymes and then excreted. Other enzymes, including flavin monooxygenases (FMOs), alcohol and aldehyde dehydrogenases, and monoamine oxidases (MAOs), also aid in phase I detoxification. In phase II, toxins are conjugated into water-soluble substances, increasing their solubility, and enhancing excretion.

Ideally, phase I and phase II processes function optimally, and we eliminate these unwanted substances. Nutrient deficiencies can hinder detoxification because vitamins and minerals act as cofactors in the enzymatic pathways of phase I and phase II. One study found that detoxification of bisphenol A (BPA) depended on retinoids (vitamin A derivatives).¹ The enzymatic activity needed to eliminate BPA required retinoid stores in the liver.

Some people have genetic polymorphisms that make detoxification more challenging or simply face an overwhelming deluge of toxins, making it impossible for their bodies to manage.

Consider acetaminophen (paracetamol), a popular pain reliever. The most common cause of liver toxicity in the U.S. is acetaminophen toxicity due to a phase I/phase II imbalance.² A small portion of the drug is transformed into a toxic metabolite, N-acetyl-p-benzoquinoneimine (NAPQI) and then conjugated with glutathione using GST during phase II. In toxicity cases, the system gets overwhelmed, and the drug converts into NAPQI, depleting glutathione stores and causing liver damage. To counteract rising levels of NAPQI, glutathione, or N-acetyl-cysteine (NAC), a precursor to glutathione, is often administered after an acetaminophen overdose. NAC's success in reversing acetaminophen hepatotoxicity has led to its use in reversing non-acetaminophen liver failure.^3,4

Our bodies can naturally handle the occasional toxin. However, when much of what we eat, drink, and breathe is laced with non-nutritive substances, our bodies need extra nutritional support to bolster our detoxification pathways. Incorporating allergen-free proteins like collagen can support this process, providing necessary nutrients without introducing additional toxins.

NutriClear® Plus is a science-based metabolic cleanse program. It is offered in a delicious-tasting powder and promotes safe and effective detoxification through its powerful combination of clean protein micronutrients, the phytonutrient-rich NitroGreens® blend, and fiber, fruit, and vegetable extracts.

References:

1. Igor O Shmarakov, Vira L Borschovetska, William S. Blaner, Hepatic Detoxification of Bisphenol A is Retinoid-Dependent. Toxicol Sci. 7 May 1;157(1):141-155.
2. Anne M Larson, Julie Polson, Robert J Fontana, Timothy J Davern, Ezmina Lalani, Linda S Hynan, Joan S Reisch, Frank V Schiødt, George Ostapowicz, A Obaid Shakil, William M Lee; Acute Liver Failure Study Group. Acetaminophen-induced acute liver failure: results of a United States multicenter, prospective study. Hepatology. 2005 Dec;42(6):1364-72.
3. B H Lauterburg, G B Corcoran, J R Mitchell. Mechanism of action of N-acetylcysteine in the protection against the hepatotoxicity of acetaminophen in rats in vivo. J Clin Invest. 1983 Apr;71(4):980-91.
4. Tauseef Nabi, Sumaiya Nabi, Nadeema Rafiq, Altaf Shah. Role of N-acetylcysteine treatment in non-acetaminophen-induced acute liver failure: A prospective study. Saudi J Gastroenterol. 2017 May-Jun;23(3):169-175.