Fruits and Vegetables Aren't Good for Every Body All the Time.

B) Toxins

Many people are not aware that individuals can be intolerant of an entire class of biochemicals due to an inability to metabolize that class or may be more prone to tissue damage because of an imbalance in the body's ability to transform and eliminate certain types of molecules. These are not immune responses like allergies.  If the body is not able to fully process a particular molecular form, it can eventually become toxic because concentration surpasses elimination or because metabolic byproducts are damaging.

There are two main categories of toxic molecules: endogenous and exogenous.  Endogeneous molecules ("internal producing") are substances that are the result of the body's natural processes; they are produced inside a cell or organ. These include, for example, the interim amino acid metabolite homocysteine or reactive oxygen or reactive nitrogen species (ROS and RNS respectively), which are free radical oxidants that can damage tissue, and peptidoglycans, which are a waste products of our gut microbiota.

Exogenous molecules ("external producing") are substances produced outside the body and affect us through our exposure to them. This refers to the chemicals in our natural environment with which we have been living for hundreds of thousands of years.  Over the course of millennia, we have evolved functional enzymes to utilize, transform and eliminate these molecules.

Our food is a major source of exogenous molecules, but so also are certain food additives, ionizing radiation and smoke, vapor and exhaust from burning hydrocarbons (plant matter or petroleum). At higher concentrations, or by using a natural chemical in a new way in our industrial age, exogenous molecules can harm tissue. 

For example, antinutrients from fruits and vegetables can be directly toxic or interfere with the absorption of other nutrients: urushiol-raw cashews; hydrogen cyanide-raw cassava; caramboxin-starfruit; solanine-over-rip potatoes; and phytic acid, lectins and saponins from seeds, nuts and beans.

Damage can also arise from the creation of reactive oxygen species as a result of the metabolic process of breaking down these external chemicals.  When this metabolic process is compromised, the combined effect of increased ROS production from internal and external sources can lead to tissue damage.

A specific category of exogenous molecules are known as xenobiotic ("foreign to life").  These are invented molecules synthesized by humans and not normally present in living organisms or in the planet's environment.  This may include drugs, industrial chemicals for manufacturing and pesticides on our food. Some chemicals normative to one species may be considered xenobiotic if it is taken up by another species.

Xenobiotic chemicals can be carcinogenic (cancer-causing) or create major tissue or organ harm, depending upon the chemical and amount and length of exposure. For example, the health dangers of glyphosate to our intestines, a weed-killer used extensively in a large-scale agriculture, is most recently known. Due to its prevalence in the industrial food system, our exposure to it has far outpaced our ability to process it.

Over the eons, our bodies generally developed the ability to produce and use or transform and eliminate endogenous and exogenous molecules so that we gain benefit from them and are not harmed by them.  But harm can result from two basic causes: increase in the production of endogenous molecules and/or decrease in the ability to transform and eliminate endogenous, exogenous and xenobiotic molecules after production or exposure, or to repair damage after production or exposure.

The increase or decrease can result from dysregulation among some of the many functional enzymes that are responsible for managing the impact of these chemicals on our bodies.  One reason for enzymatic dysreguation is genetic mutations that cause enzymes to under-perform, over-perform or mis-perform, which imbalances the body's ability to regulate certain chemicals healthfully.

Tx Genetic Research investigated the presence of symptoms of toxicity associated with fruit and vegetable consumption due to genetic variants diminishing the function of Phase II liver enzymes. This toxicity was further associated (but not exclusively so) with diminished epithelial mucosa tissue function (see Nutritional Trial Results).

The general assumption among medical and health researchers is that the natural chemicals in fruits and vegetables are by themselves too mild in concentration to be problematic. However, there is scientific recognition, to a greater or lesser extent, of certain aspects of a toxic relationship between metabolism of exogenous chemicals in fruits and vegetables and damage to epithelial mucosa tissue.


1. A sensitivity to salicylate (a form of salicylic acid) is one of the most well known examples of this phenomenon. 

Salicylate is the most prevalent molecule of the phenolic acid biochemical family (itself a form of aromatic ring hydrocarbon) in fruits and vegetables, and in some drugs like aspirin. Systemic symptoms of salicylate toxicity may include:

Mild: Itchy skin, hives, rashes; red or white bumps or skin patches; sore, itchy or burning red eyes; dark circles under the eyes; nasal or sinus congestion, nasal polyps; red flush in face and ears; ringing in the ears, tinnitus; extra thirst, water difficult to retain, frequent urination; urination urgency; eye sensitivity to light, skin sensitivity to sunburn; odorous bed clothes and body.

Moderate: Swelling of hands, feet, eyelids, face or lips; joint inflammation; irregularly occurring fever; stomach cramps, nausea, vomiting, diarrhea or constipation; heart palpitations, arrhythmia, tachycardia; asthma, persistent coughing, wheezing; headaches, dizziness; poor concentration, periodic fatigue; insomnia; heavy perspiration, night sweats.

Severe: Behavioral swings between high energy and feeling upbeat, and low energy and feeling downbeat; mood swings between depression and anxiety; chronic fatigue; irritability, aggression, self-injury; distractible, overactive, fussy, hyperactive; brain fog, sluggish thought process, lack of clarity, confusion, memory loss, blood pressure changes.

Most severe: hallucinations, seizures, coma, death.

Salicylates are circulated within the body for use, transformation and eventual elimination by attaching to two enzymes, the long-named UDP glucuronosyltransferase 1 family, polypeptide A cluster (UGT1A) and phenol sulfotransferase 1A (SULT1A).

2. A number of researchers have noticed that these systemic reactions may not be limited to salicylates but may apply to the total class of phenolic acid compounds or to other food biochemicals. 

The Feingold Diet, based on the 1970s research of Dr. Benjamin Feingold, focused on eliminating salicylates and artificial food flavors and colors ( for children with ADD/ADHD.

Dr. Rosemary Waring investigated in 2000 the association of phenol toxicity with a decrease of phenol detoxification in autistic children due to an insufficient supply of sulfate, which is necessary for the production of phenol sulfotransferase 1A. ( and

More recently, the Failsafe Diet, devised by Sue Dengate (, is based on the chemical exclusion diet developed by the allergists at the Royal Prince Albert Hospital in Australia ( It focuses on eliminating salicylates, amines (from processed and aged protein foods) and glutamate (in the flavor enhancer monosodium glutamate and in large doses of protein foods) to avoid toxicity from all these food sources.

3. Tissue damage from aromatic ring hydrocarbons, the molecular basis of petroleum, is a well-established fact.

Here are two research reports out of hundreds that denote how aromatic hydrocarbons (in these reports, benzene) can damage epithelial tissue. There are many enzymes responsible for metabolizing aromatic hydrocarbons in the body.

First, aromatic hydrocarbons in the form of diesel exhaust particulates cause epithelial damage in the lungs:  "Organic diesel exhaust particle chemicals also induce apoptosis and necrosis in bronchial epithelial cells via a mitochondrial pathway. This may be responsible for epithelial shedding and bronchial hyperreactivity in asthma" (Nel+ 2001). 

Second, "[h]igh concentrations of benzene induce an inflammatory response and possibly fragmentation of DNA in respiratory epithelial cells" (Gosepath+ 2003). 

Nel, Andre E. MD, PhD; Diaz-Sanchez, David PhD; Li, Ning MD, PhD, The role of particulate pollutants in pulmonary inflammation and asthma: evidence for the involvement of organic chemicals and oxidative stress, Current Opinion in Pulmonary Medicine: January 2001, Volume 7, Issue 1, p 20-26.

Gosepath J., Grebneva N., Brieger J., Mann W.J., Evaluation of Inflammatory Reactions and Genotoxic Effects after Exposure of Nasal Respiratory Epithelia to Benzene, Journal for Oto-Rhino-Laryngology, Head and Neck Surgery, 2003; 65: 348–352.

A) Allergens

C) Pathogens and Biotoxocity

D) Autoinflammation and Autoimmunity

Helen C Harrison, M.A.

Consultant, Educator, Researcher, 951-438-5531

The FDA has not reviewed the contents of this website. This information does not claim to prevent, diagnose, treat or cure any medical condition. It is provided for educational purposes.