Toxins and Their Causes

Toxins are organic poisons produced by animals, plants, or bacteria and can cause certain diseases. Research shows that toxins have become a primary cause of chronic disease. Toxins include not only metals and chemicals in the environment but also autogenously produced toxins such as those from homocysteine (an amino acid in the blood), gut bacteria and hormones that were not fully detoxified. To add to this list are what is referred to as toxins of choice such as intentional exposure to pesticides, polychlorinated biphenyls (PCBs), phthalates or plasticizers (used to make plastics more flexible), or mold from humid buildings. Also, some people intentionally consume toxins that include alcohol, salt, corn syrup, nonsteroidal anti-inflammatory drugs (NSAIDs), and even gluten. The enormous load of all toxins that people are exposed to or intentionally consume add up may result in physiological and structural damage, and over time, may also lead to chronic conditions.

Common chronic conditions are the leading causes of mortality in developed countries and are becoming predominant in developing nations. Chronic conditions include cardiovascular disease, obesity, diabetes, metabolic syndrome, neurocognitive disorders, immune dysfunction, and cancer. Chronic disease is debilitating some economies due to upsurge in healthcare costs, persistent individual suffering, tormented families caring for afflicted loved ones, and curtailed opportunities as employees get sick and are not productive.

NDL-PCBs and PCB Congeners 126 and 153

The effects of PCBs were examined in individuals exposed to these compounds through diet, work environment, and industrial accidents. PCBs are considered a carcinogen, and they are related to the biliary tract, liver, skin, liver, and intestinal cancers. Other effects of PCBs may include abdominal pain, nausea, vomiting, eye irritation, respiratory problems, increased susceptibility to infection, and hypothyroidism. PCB exposure may also result in menstrual irregularities and fertility decline in women. 

PCBs were used as lubricating and cooling agents in transformers and electronic equipment because of PCB’s high resistance to heat. However, PCBs do not break down in the environment and accumulate in the bodies of animals and humans. The use of PCBs was already banned by the Environmental Protection Agency (EPA). Despite that, PCBs still persist, and they continue to  

PCBs were banned from use in the US in 1979 by the Environmental Protection Agency (EPA). However, PCBs continue to leak into soil and groundwater from hazardous landfills. Since PCBs accumulate inside the bodies of living organisms, humans are exposed to the toxins from PCB whenever they consume food sourced from areas where food are considered contaminated.

Polychlorinated biphenyls (PCBs) are a mixture of individual chemicals. They can be divided into two groups, according to their biochemical and toxicological properties: the dioxin-like PCBs (DL-PCBs) and the non-dioxin-like PCBs (NDL-PCBs). More than 90% of human exposure to NDL-PCBs is through food.

In chemistry, congener means a member of the same taxonomic genus as another organism. A study investigated the effect of two congeners of PCB, PCB153 and PCB 126, to progesterone and testosterone. PCB153 is one of the most prevalent environmental contaminants, while PCB 126 is one of the most toxic contaminants similar to dioxin. In another study, acute exposure to PCBs 126 and 153 was found to have some effects on the pituitary and thyroid hormones in adult male rats.

The PCB Toxicity Test

Symptoms of PCB exposure include fatigue, eye irritation, severe acne, rashes, obesity, allergies, liver damage, weak immune system, and some developmental disorders. The PCB profile can help determine the identity of the most toxic PCB exposure that a patient has experienced. The national reference ranges of the commonly found PCBs have also been documented to include the adverse health problems that they may cause. Levels are given both in parts per million or PPM and as lipid-adjusted amounts to allow the clinician to give the best estimate of the total body burden of these compounds.

Once PCBs enter the body, the fat cells absorb and store them. Since PCBs does not dissolve in water, they are not excreted from the body and over time, they accumulate. Polychlorinated biphenyl testing can help one determine the extent of this PCB burden.

A PCB toxicity problem affects children more than adults. A lowered immune system can lead to complications in children, such as sensitivities, allergies, and chronic infections. Still, a heavy concentration of PCB toxins in adults over time may cause impairments in the brain, nervous system, immune system, and endocrine system. PCB toxicity may also cause fertility issues.

Is CBD Toxic?

CBD is Non-Psychoactive

CBD or cannabidiol is a chemical compound that is naturally found in a cannabis plant, which may be marijuana or hemp. Hemp is predominantly CBD and contains less of tetrahydrocannabinol or THC, the intoxicating substance. Marijuana, meanwhile, contains a high content of THC, which is responsible for inducing a sense of euphoria or “high” that users experience when they smoke or consume it. Studies and research have been conducted on the subject of CBD’s non-psychoactive properties. Since 2010, researchers have confirmed the role of CBD in treating different symptoms of diseases and disorders without causing intoxication.  

CBD is Non-Addictive

The World Health Organization (WHO) released a report that demonstrates how CBD passed tests that examined whether or CBD has the potential for abuse. Volunteers were given CBD, and then they were assessed using a series of tests. WHO declared that CBD oil is not addictive since the volunteers did not manifest signs of possible abuse or dependence on CBD. The result of this investigation is excellent news for people who are skeptical and worried that CBD might be habit-forming in a destructive way.

CBD is Bi-Phasic

CBD is bi-phasic, meaning it produces unique effects for any individual user whenever the amount of CBD consumed is substantially elevated or reduced. When CBD is taken in small doses, users typically experience an energizing effect. However, when CBD is taken in high doses, the effects are comparable to that of a sedative.

Benefits of CBD

Cannabidiol has been proven to be a great medication for various health conditions. The use of CBD oil is generally safe and does not lead to dependence or tolerance towards the drug. CBD is an ideal choice for those trying to combat addictions or refrain from using addictive drugs.

One of the most popular benefits of CBD use is relief from chronic pain and inflammation. Individuals suffering from chronic pain due to fibromyalgia have experienced relief after using CBD oil. In Canada, CBD has been approved for the remedy of cancer pain and multiple sclerosis.

CBD calms epilepsy. The US Food and Drug Administration (FDA) has approved the prescription use of Epidiolex, a purified form of CBD oil. Epidiolex can help treat Lennox-Gastaut Syndrome and Dravet Syndrome, two rare and severe forms of epilepsy that do not respond to anti-seizure medications.

CBD, a non-psychoactive compound, can also help decrease anxiety levels in people with anxiety-related behavioral disorders. CBD’s antioxidant and neuroprotective characteristics may also reduce neurological damage caused by free radicals, thereby reducing oxidative stress. CBD is also observed to help prevent blood pressure changes due to stress. CBD also has an outstanding ability to destroy bacteria, especially drug-resistant strains. 

CBD, when used as a medication to common ailments and disorders, exhibit fewer side effects compared to conventional medications. Although more research is required into the benefits of CBD as a therapeutic agent, more people are turning to CBD to manage or alleviate their symptoms. For people with irritable bowel syndrome or IBS, CBD oil may offer a safe alternative solution. A study demonstrates that CBD can relieve some forms of constipation. The proper use of hemp seed pills may benefit those who want to avoid constipation or are hoping to use an alternative natural remedy for this digestive problem. 

The Endocannabinoid System 

Cannabinoids are compounds found in cannabis, and they have demonstrated diverse and severe effects on the body systems, which could lead to modifications of the body’s physiological functions. Cannabinoids play a critical role in the introduction of immune, respiratory, carcinogenic, and reproductive. The probable toxicity related to the prolonged use of cannabinoids works as a tumor promoter in animal models and humans. Some synthetic cannabinoids have low compatibility with CB1 or CB2 receptors, unlike Δ9-THC, which has a strong affinity towards these receptors. Cannabinoids and their derivatives have a direct or indirect interconnection with acute and long-term toxicity. 

The endocannabinoid system (ECS) is a complicated cell-signaling system discovered by researchers exploring THC (tetrahydrocannabinol), one of the most-recognized cannabinoids. Experts are still trying to fully comprehend the ECS aside from its critical role in regulating a variety of functions and processes such as mood, memory, sleep, appetite, and reproduction. The ECS naturally occurs and is active in the body with or without the consumption of cannabis. The system’s primary components are the endocannabinoids, receptors, and enzymes.

Endocannabinoids are molecules produced by the body, and they are called endogenous cannabinoids. The two identified endocannabinoids are AEA (anandamide) and 2-AG (2-arachidonoylglyerol). They both help maintain body functions operate smoothly. However, it is difficult to determine the typical levels for each of them as the body generates them as needed.

The endocannabinoid receptors are found throughout the body. Endocannabinoids adhere to them to prompt the ECS to perform its function. Endocannabinoids can bind to either of the two main endocannabinoid receptors. CB1 receptors are mostly situated in the central nervous system, while the CB2 receptors are mostly found in the peripheral nervous system. The results of the binding of these receptors with the endocannabinoids are dependent on the location of the receptor and which endocannabinoid it attaches to. As an example, endocannabinoids might aim for CB1 receptors in a spinal nerve to alleviate pain. In another instance, endocannabinoids might target a CB2 receptor to signal inflammation, a typical indication of autoimmune disorders.

Toxicity of Cannabinoids

Short-term exposure to cannabis causes minimal toxicity, without causing death due to direct or immediate use of recreational herbal medicine. The most pronounced reported effect of short-term exposure to cannabis would be on the cardiovascular system, which demonstrates substantial elevation of heart rate and decrease in blood pressure. Also, heavy usage of cannabis may damage the intellectual and cause psychomotor function impairment stands lasting up to 48 hours after taking cannabinoids.

On the other hand, studies have shown that the extensive uses of cannabinoids have long-term effects on brain functions. Cannabis has shown to induce effects on an individual’s psychomotor performance, attitude, sleep, memory, ECG (electroencephalogram), heartbeat, and body temperature. The withdrawal symptoms of cannabis are linked to that of alcohol and opioids such as sleeplessness, anorexia, nervousness, muscular tremors, and dysphoria. The common indications also include salivation, nausea, weight loss, and loose bowel movements. 

Because of the minimal quantities of cannabinoids that are released from the fatty tissues into the bloodstream, observing cannabinoids toxicity remains to be a challenge.  Initial exposure to cannabis with a single dose or overdose produces psychological effects like anxiety, mania, fear, and illusion. Cannabinoids may also result in life-long psychotic effects that include including hallucinations which may be misdiagnosed as schizophrenia. Although the effects of cannabinoids are not life-threatening, cannabis medication should not be prescribed in these individuals, which may aggravate toxicity when used in conjunction with other drugs due to drug interactions. 

Studies into CBD’s chemical characteristics have not found any evidence of a fatal overdose. The National Cancer Institute, posted on its official website that because cannabinoid receptors, unlike opioid receptors, are not situated in the brainstem areas regulating respiration, fatal overdoses arising from excessive consumption of cannabis and cannabinoids do not occur. 

Medical Marijuana Becomes Toxic

A study was conducted on the use of medical marijuana by those whose immunity is compromised by AIDS or cancer chemotherapy. Researchers found that medical marijuana may help to alleviate symptoms of the disease or therapy.

When marijuana is burned, it produces creates toxins of combustion. The use of a vaporizer reduces the number of toxins or tars. The water pipes function as filters to the gas-phase toxins. However, water pipes also filter some of the THC or tetrahydrocannabinol content, making this strategy counterproductive. Fungal spores in marijuana may be the cause of the most considerable risk to immunocompromised patients. Several methods may sterilize fungal spores. However, pesticide residues and other contaminants may be present in marijuana sold in the market.

CBD and Liver Health

The market for products with ingredients that include cannabidiol or CBD, the non-psychoactive, pain-relieving chemical in cannabis, has been on the upsurge in recent years. CBD products are becoming increasingly popular among those who seek a natural remedy to specific disorders or ailments. However, CBD is still relatively understudied. The U. S. Food and Drug Administration (FDA) has warned the public against unscrupulous manufacturers that make claims which are not supported by scientific evidence.

A Study on Mice

A study investigated the hepatotoxicity of a cannabidiol-rich cannabis extract in a mouse model. The researchers’ findings suggest that excessive consumption of CBD might lead to liver damage has caused alarm among cannabis proponents. However, some experts argue that the study conducted on a small sample of mice model does not provide substantial support to that claim.

There is a lack of complete and extensive toxicological studies on the safe use of CBD. These studies are needed for marketing CBD and products containing CBD. Researchers from the University of Arkansas examined some of the effects of administering various doses of CBD on a group of 8-week-old mice. The mice that were given large doses of CBD, equivalent to giving 200 mg of CBD in humans. Researchers found that while the mice exhibited tolerance of these high doses, the animals also demonstrated apparent signs of liver toxicity. Moreover, repeated doses of small quantities of CBD resulted in liver swelling and damage. The low dose that was given to the mice is equivalent to 50 mg CBD in humans.

A 200 mg dose is not applicable to most real-life situations. However, the data provided critical information concerning the possible consequences of CBD overdose. The authors of the study published in the journal Molecules also explained that the data they gathered during the experiment could be used as the basis for doses needed for further toxicity-related studies.

However, a big caveat to this study is that the mice were given doses that in humans were equivalent to the maximum recommended dose of the drug Epidiolex. Epidiolex is a specific prescription drug that is administered to patients to treat seizures.

To put the results of the study in perspective, the CBD dosage that was given to the mice in the study is comparable to over 1,300 mg of CBD per day for an adult with a bodyweight of 150 pounds. This dose is much higher than the typical daily dose of typical CBD oil users. Most people maintain a regular dose of 10 mg to 80 mg per day, with slightly higher doses for insomnia and therapeutic effects. Currently, there is no federal regulation for many CBD products sold in the market, so one cannot rely on the contents of a substance as described on the product label. The FDA sent warning letters to manufacturers that sell their products with inaccurate levels of compound that do not match what is listed on the packaging. 

The label on the packaging of Epidiolex gives a warning for liver injury. It explicitly states that the patient or user should monitor his or her liver enzyme levels. 5% to 20% of patients in clinical trials developed a substantial increase in liver enzymes, and some patients were withdrawn from the experiment. Researchers concluded that anyone consuming CBD consistently and in extreme doses might eventually experience liver damage or liver disease. 

On the other hand, there are studies that corroborate the fact that cannabis may be beneficial in treating liver damage.  

Clinical Studies on Cannabis vs Liver Damage

Study shows that cannabis use is linked to the reduced pervasiveness of progressive stages of alcoholic liver disease (ALD). The study was conducted to determine the effects of cannabis use on the occurrence of liver disease in individuals who consume alcohol in excessive quantities.  While cannabis has exhibited anti-inflammatory characteristics, the connection between CBD use in conjunction with alcohol and the development of liver disease remains unclear. 

A similar study shows the association of marijuana use with non-alcoholic fatty liver disease (NAFLD) among adults in the United States. Researchers concluded that contemporary marijuana use might favorably impact the development of NAFLD. Current or active marijuana use was related to a lower risk of NAFLD, independent of metabolic risk factors. These data suggest that cannabinoids should be explored as a probable strategy for the treatment or prevention of NAFLD. However, until further evidence is gathered, no recommendations can be made regarding the clinical application of marijuana in patients with NAFLD. 

In another study, patients maintaining cannabis consumption after 3 years presented the smallest increase in (fatty liver index) FLI over time. The increment was significantly smaller than that of the FLI of people who discontinued their cannabis consumption. Researchers concluded that cannabis consumption might produce a therapeutic effect against liver steatosis, probably through weight management.

Study shows that the use of cannabinoids with Alcoholic Liver Disease (ALD) may have a possible therapeutic effect. In a mouse model, the animals demonstrated reduced inflammation, oxidative stress and hepatic steatosis (accumulation of fat in the liver) with cannabis use

Safety Concerns with CBD

Patients should always be wary of making any changes in their diet, lifestyle or medications, including CBD. However, there are situations when CBD may not be conducive to a healthy treatment program.

CBD is still unregulated, and its proper dosage is still not determined. More studies need to be conducted, and the investigation has to be done on more subjects in clinical trials for extended periods. Most studies were conducted on a small number of individuals for only two weeks long. For example, several aspects of the investigations on CBD’s toxicity are still scarce. Studies on CBD’s interactions with other pharmaceutical drugs in clinical set-ups have to be performed. Still, there is data that suggests that CBD is well-tolerated up to 1,500 mg daily.

Compared to the adverse effects of THC, the side effects of CBD oil are milder and rarer. One may experience a mild headache or feel a bit lethargic as the effect of CBD wears off. To avoid these undesirable effects, one has to lower his or her CBD dosage. However, one must refrain from changing his or her brand of CBD product because it makes the effects more unpredictable. The typical side effects of CBD oil are dizziness, nausea, vomiting, dry mouth, diarrhea, and changes in appetite. Still, CBD dosage is unique for every individual.

Variation in THC Content

CBD oil, in its pure form, is an excellent medication. However, the exact chemical structure of the different CBD products available in the market is often inconsistent, posing a threat to human health. This variation in chemical composition is due to the presence of THC or Tetrahydrocannabinol, along with several contaminants. While the benefits from CBD use may be derived from initial use, it is probable that with prolonged use, the medical conditions being treated may further aggravate because of the THC content. It is also possible that a patient may develop additional issues that were not present before.


Another cause of concern is the rampant cases of mislabeling of DBD products in the market. According to a research paper, almost 70% of all CBD products sold online are not labeled accurately. Some products may contain higher traces of THC than what is legally permitted, which is only up to 0.3% THC content in industrial-grade CBD or hemp oil.


The presence of contaminants in many CBD products also poses some health hazards unbeknownst to CBD enthusiasts. Some studies have pointed out that cannabis plants from unregulated sources often carry contaminants that are detrimental to human health like pesticides and metal particles. 

Industrial and agricultural pollution may cause contamination, as well. Common heavy metals found in soils include nickel, zinc, manganese and copper. However, more harmful metals like mercury, arsenic, lead, and cadmium can also be found in high concentrations in the soil. These contaminants are passed on from the soil to the plants.

Sample Cases of Contamination

Sometimes, contaminants are deliberately added by manufacturers to increase the yield, weight, or potency of the product. On other occasions, these contaminants accidentally get mixed in the products due to carelessness and the lack of strict regulations regarding the production of CBD products.

In one case, a paper from the Netherlands Ministry of Environment and Health recently revealed that of all the cannabis sold in coffee shops in their country, at least 90% contains traces of illegal crop protection products, such as pesticides.

In another case, pesticides were found in cannabis marketed under state law in California and medicinal cannabis from licensed producers in Canada.

Unintentional contaminants like heavy metals, molds, and bacteria, have also found to be mixed with some CBD products.  Results from a report suggest that gamma irradiation of herbal cannabis remains the recommended method of decontamination.

Gamma irradiation is a physical or chemical process of sterilization that destroys bacteria by breaking down bacterial DNA, preventing bacterial division. The gamma irradiation sterilization method does not involve adequate energy to cause the treated products to become radioactive. The process only harms the microorganisms on the products. Moreover, this decontamination process does not rely on humidity, temperature, or pressure and can be practical to use on packaged goods.

Interaction with Other Medications

CBD may interact with other prescription medications that one may be taking with it. Although in some cases, CBD has been seen to boost the therapeutic effects of some prescription drugs, it is still unsafe to take CBD in conjunction with other drugs for the treatment of any disease. The cause of this concern stems from the fact that the CYP450 liver enzyme, which metabolizes these drugs, is also the same enzyme that breaks down CBD in the bloodstream. There are risks involved when high levels of concentration of these drugs accumulate in the bloodstream, causing unwarranted side effects of drug interactions or a potential overdose.

Drugs that need the CYP450 enzyme to metabolize include antihistamines, steroids, antibiotics, anesthetics, antidepressants, benzodiazepines, beta-blockers, anti-seizures, and antipsychotics. These drugs may not always react adversely with cannabidiol oil, but precaution is still advised.

CBD and CYP450

CBD and other plant cannabinoids have the potential to interact with many pharmaceuticals by impeding the functions of cytochrome P450. This significant enzyme group metabolizes most of the drugs that the body consumes, including more than 60 percent of medicines in the market.

In a study, researchers found evidence to suggest that at sufficient dosages, CBD would temporarily neutralize cytochrome P450 enzymes. When these enzymes are deactivated, the breakdown of a wide variety of compounds, including tetrahydrocannabinol (THC), is also altered.

However, Dr Kazuhito Watanabe, in a presentation that he made at the 2015 International Cannabinoid Research Society convention, indicated that cannabidiol might induce or meaning intensify the activity of some cytochrome P450 enzymes. Based on the evidence gathered in both reports, one may conclude that CBD may either strengthen or weaken the metabolism of other drugs, depending on the particular drug used and the dosages applied.

The Fear of CBD Overdose

An individual cannot overdose on CBD, and no evidence has ever suggested that one can overdose on the intoxicating cannabinoid THC. A World Health Organization report concluded that CBD is “generally well tolerated with a good safety profile.” Human subjects in the studies have reported some side effects, such as drowsiness, lack of appetite, diarrhea, lethargy, convulsions, vomiting, and abnormal tests results on liver function.

So far, there has been no apparent limits to how much CBD is too much CBD. Therefore, the best advice for patients who are unsure of CBD dosage is to start with a minimal dose, gradually increasing to a higher dose over time while observing how the body reacts to CBD. Effects that were reported in relation to CBD use could have been induced by the adverse effects of an interaction between CBD and the individual’s existing medications. Once an individual reaches a level that makes him or her feel significantly better, that dosage could be his or her maximum dose. However, if one begins to experience a worsening of health conditions, he or she should scale back the dosage a little, as the optimal dosage could have been already reached. 

Factors to Consider When Purchasing CBD Products 

Although CBD oil is non-intoxicating and generally safe, one still needs to take precautionary measures when consuming it. Being well-informed of one’s CBD product source, as well as limiting oneself to a particular dosage, is crucial to benefit from CBD fully. Not every CBD vendor is trustworthy and reliable. Neither is CBD legal in all places. Several regulations and conditions apply in some states with regards to CBD use. There are several factors to consider to ensure the safety of the CBD products purchased.

  1. One must research on the exact legal stipulations applicable to CBD in his or her area.
  2. Buyers of CBD products must only purchase from legitimate and reliable big brands.
  3. When buying from an online store, the buyer must research product reviews. When buying from a physical store or dispensary, he or she must check whether the store is authorized by the government to sell CBD.
  4. One important thing to look for in CBD products is certification codes. Several certification authorities approve certain products only after some thorough screening tests. 
  5. Buyers must also compare company claims about their products’ potency with that of the third-party lab reports. 
  6. Consulting a trusted medical professional who is experienced in CBD use is ideal before one purchases his or her first bottle of CBD. 

CBD Dosage Guidelines

Doctors advise patients who are about to commence a CBD therapy, to start with a small dose. Doses of up to 1500 mg daily are relatively safe and beneficial for humans. Doses of up to 300 mg a day can be used without any health risks for up to 6 months. Doses of 1200 mg to 1500 mg a day can be safely consumed for up to 4 weeks or one month. In sublingual applications, 2.5 mg a day of under-the-tongue sprays can be safely used for up to 2 weeks.

Small Doses vs Large Doses

Doses of 1 mg to 20 mg are considered small doses, while anything above 50 milligrams is safely considered a large dose. Still, the size of the dosage is dependent on the user’s body weight, physical condition, and the period of usage, among other factors. Someone may need at least 50 mg of the CBD to experience any therapeutic effect at all. In such a user, sedative effects may be felt only after consuming a dosage over 100 mg. However, clinical tests on humans are conducted with a higher dose of CBD (up to 1000 mg), with almost no side effects at all. Results of a study provided evidence that CBD dosage of up to 1,500 mg a day is well-tolerated by humans. 

Even when consumed in high amounts, there has been no reported incident that one can overdose on CBD. CBD does not interact with the brain receptors that control heart rate and breathing. However, if there are any side effects of CBD overdose, they are very minimal and of minor importance. Most of the common side effects are drowsiness, low blood pressure and dry mouth.

CBD Oil for Pets

CBD oil is considered safe for pets like dogs and cats. CBD has been broadly tested on both animals and humans in clinical trials, and it is widely used as a therapeutic supplement. While there has been no official ruling from the U. S. Food and Drug Administration on CBD, there is no corroboration that CBD is detrimental to humans or animals. One should keep in mind that CBD is a natural cannabinoid. Hence, the bodies of pets, such as dogs and cats, naturally produce their own cannabinoids to interact with the endocannabinoid system or ECS. Both CBD and a dog or cat’s naturally produced endocannabinoids are capable of interacting with the ECS. Regulation of the ECS would help maintain the optimum level of homeostasis (stability or balance within the body) in dogs.

CBD products in different forms can be taken by dogs or cats. There are CBD oil drops, which can be added to pet food or water or directly in the pet’s mouth. CBD-infused dog treats and CBD-infused cat treats are also available, as well as CBD capsules available for pets. The capsules make travelling with pets hassle-free, and they are perfect for fast, accurate dosing.

CBD is not psychoactive, so it would not induce a high in one’s pets. There is no known toxic dose of CBD and no reports of any people or animals overdosing on CBD. Like any supplement, there is a point at which administering additional CBD would yield no added benefits advantages. It is always recommended, therefore, to give a dog small amounts of CBD first and then monitor the effects before increasing the dosage. CBD dosage is primarily given to pets according to the animal’s body weight. However, the dose may also be determined by the severity of the symptoms or disease being treated.


The key to determining one’s CBD dosage is the careful observation of how the substance impacts one’s well-being.  Everybody is unique. People may have different reactions to CBD, depending on the quantity consumed. Since researchers have not identified any precise doses or limits, the best way to commence one’s CBD regimen is to start with a low dose. As one gets accustomed to the effects of CBD, a gradual increment in doses may be applied until one experiences the full benefits of CBD. A careful examination of how one’s body reacts to CBD must be noted. Consulting with a medical professional experienced with cannabis would be best. 

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Potential Sources of Toxins

  1. Atrax Robustus

    Sydney funnel web spider is the common name of Atrax robustus. While the majority of funnel web spider bites, even by the proven lethal Atrax robustus, are minor and without systemic envenomation. When severe effects do occur, they may prove difficult to treat and end fatally.  Antivenom has had a significant effect in reducing the likelihood of fatal outcome. Only Atrax robustus is a proven cause of fatalities. It is now established that Hadronyche formidabilis, H. infensa, H. versuta, H cerberea, Hadronyche spp.7 can cause dangerous bites in man. For most other Hadronyche spp there is no present evidence that they are dangerous to man, though this may merely reflect the infrequency of bites.  Male Atrax robustus are generally more dangerous than females. This may not be true for all species.

    Main risks are cardiovascular disturbance; pulmonary edema; acid-base disturbances; intracranial hypertension (proven in monkeys, not in man). Target organs: envenomation causes a complex multi-system disease involving the cardiovascular system, lungs, central nervous system and peripheral nervous system including the autonomic and neuromuscular systems.

    The bite of Atrax robustus causes severe local pain, in part due to mechanical injury from large powerful fangs.  Some local erythema may develop. The pressure-immobilization method is the only recommended first-aid and has been proven effective in studies with monkeys, and in clinical experience. Maintain life with cardiopulmonary resuscitation measures as indicated. Reassure and rest the patient. Remove Atrax robustus spider if still attached, ensuring no further bites occur. Immediately apply a firm broad constrictive bandage (such as crepe) over the bite site at the same pressure as for a sprained ankle.  Extend the bandage to cover as much of the bitten limb as possible, at the same pressure (ie, the bandage should NOT act as a tourniquet).

    All known cases of human envenomation are due to bites. (Sutherland 1983) Onset of systemic envenomation may occur from 10 minutes up to an hour or more after the bite (with further delay if appropriate first aid used). Earliest systemic symptoms are usually tingling around the mouth which often occurs within 15 mins of the bite, tongue spasms, followed by nausea and vomiting, abdominal pain, profuse sweating, brisk salivation, lachrymation, and severe dyspnea. The level of consciousness may rapidly deteriorate, with confusion or coma. Hypertension is usually noted at this time. Severe pulmonary edema may develop quite early, and is a potential cause of fatality, particularly in children. The pulmonary edema is mixed in origin, similar to neurogenic pulmonary edema, with catecholamine release, high filling pressures, and membrane leak.


  2. Pseudonaja Affinis

    Pseudonaja Affinis or brown snakes are oviparous, diurnal or crepuscular, and in warm weather may be nocturnal. Food varies with species, subspecies and locality and principally comprises small lizards and small mammals. They do not possess discrete temperature-sensing organs.

    Brown snake dentition is proteroglyphous (maxilla), the paired fangs being situated in the anterior portion of the upper jaw “front fanged”), on partly mobile maxillae allowing limited elevation for strike (10-15°). The fangs have venom transport grooves, enclosed for most of their length. Average fang length 2.8 mm (2.0 – 4.0 mm), average distance between fangs 9 mm. Pupils are circular. The head is not distinctly triangular. Cogger 1975)

    Seven species are currently recognised, although some taxonomists now believe some species actually comprise a species complex, ie, P. nuchalis may comprise a complex of 5 species (Mengden & Fitzgerald 1987).

    The venom of Pseudonaja Affinis is used both in antivenom production and for laboratory research. The neurotoxins in particular may prove valuable in neuromuscular transmission research, and the procoagulants in further elucidating the mechanism of normal human coagulation.

    In human envenomation, venom is always inoculated by snake biting.  Owing to the size of the fangs, venom is most likely to be inoculated cutaneously or subcutaneously.  Experimentally, venom may be administered to test animals via subcutaneous, intramuscular, intravenous, intraperitoneal, and intraventricular (CNS) routes.

    The human lethal dose for Pseudonaja Affinis or brown snake venom is unknown. Without antivenom treatment, a few brown snake bites may be fatal (Fairley 1929a), but even in the early part of the 20th century, when neither antivenom nor ICU facilities were available, only 8.6% of reported brown snake bites were fatal. Despite this, brown snakes are still thought to be the most common cause of fatal snakebite in Australia. (Hilton 1989).

    Initially, the patient bitten by the Pseudonaja Affinis or brown snake is usually anxious. The subsequent course will depend on (a) amount of venom injected, (b) size of patient relative to venom load (ie children may be worse affected), (c) degree of activity of patient after bite (physical activity hastens venom absorption), (d) timing, type, effectiveness of first aid, (e) speed and nature of specific medical treatment given, if systemic envenomation ensues, (f) pre-existing health factors for each patient (ie past renal problems, allergic problems etc).

    Pseudonaja Affinis or brown snakes are widely distributed in most habitats of mainland Australia, but are absent form some southern islands and Tasmania.  While no high-risk geographic regions have been identified, it is evident that brown snakes may readily enter metropolitan fringes, and country towns, and are frequently found around country rubbish dumps and under the floors of elevated country homesteads, and around farm buildings.


  3. Copper Sulphate

    Copper plays an important role as a co-factor in several metalloproteins, including cytochrome oxidase and superoxide dismutase and is essential for the utilization of iron and hemoglobin formation. The richest food sources of copper are shellfish, ‘organ’ meats, seeds, nuts and grains where it is bound to specific proteins. Copper tends to exist in the cupric Cu(II) state in biological systems including water although it may also be found as Cu(I) (Linder and Hazegh-Azam, 1996). Copper deficiency is associated with neurological dysfunction and manifests as “Swayback” in lambs and calves born to sheep and cows grazing on copper deficient pastures.

    Copper sulphate is a fungicide, herbicide, commercial chemical and found in some chemistry and crystal growing sets. The anhydrous form is white, and the pentahydrate is blue. Copper sulphate is a powerful oxidizing agent and irritant to mucous membranes. A dose-response effect following ingestion is difficult to define but approximately 10 g may be fatal in an adult (Akintonwa et al, 1989).

    Chronic inhalation of copper sulphate-containing pesticides produces pulmonary and hepatic toxicity. Copper sulphate contact sensitivity is recognized.

    Symptoms of moderate or substantial ingestions include nausea, vomiting and a metallic taste within minutes, followed by abdominal pain and diarrhea. Secretions may be blue/green. Severe gastrointestinal irritation may result in hematemesis and/or melaena with hypovolemic shock. Severe poisoning is associated with the development of renal failure, intravascular hemolysis (usually manifest 24-48 hours post-poisoning) and cellular and obstructive liver damage. Methemoglobinemia, coma, convulsions, rhabdomyolysis, muscle weakness and cardiac arrhythmias are described. There is a high risk of aspiration of the gastric contents in obtunded patients.

    Copper sulphate is a powerful oxidizing agent which is corrosive to mucous membranes. Concentrated solutions are acidic (a 0.2 M aqueous solution has pH 4). Cellular damage and cell death may result from excess copper accumulation. This is likely when copper-metallothionein binding and copper clearance from the cell are blocked.

    There is no conclusive evidence that copper is carcinogenic in humans (Aaseth and Norseth, 1986). However, it is proposed that patients with “Vineyard sprayer’s lung” are at a greater risk than the general population of developing bronchial carcinoma (Villar, 1974; Stark, 1981). When originally reported in Europe, lung cancers in vineyard workers were attributed to the arsenic content of some fungicides, but in Portugal arsenic fungicides have never been used in vineyards (Villar, 1974).

    Among 14 smoking vineyard workers Plamenac et al (1985) noted atypical squamous metaplasia in four cases and suggested copper as an aetiologic agent. In a review of liver disease among 30 vineyard sprayers who had used Bordeaux mixture for three to 45 years (mean 18 years), Pimentel and Menezes (1977) observed one case of hepatic angiosarcoma. The authors suggested copper-induced sinusoidal cell proliferation as a possible trigger of tumour development.

  4. Pyrrolizidine Alkaloids

    Pyrrolizidine alkaloids (PAs) are found in plants growing in most environments and all parts of the world.  The main sources are the families Boraginaceae (all genera), Compositae (tribes Senecionae and Eupatoriae), and Leguminosae (genus  Crotalaria), and the potential number of alkaloid-containing species is as high as 6000, or 3% of the world’s flowering plants (Culvenor, 1980).  They have long been known to be a health hazard for livestock, at least since 1902 (Schoental, 1963), and loss of livestock in various parts of the world has been traced to their grazing on certain plants growing in pastures, especially following periods of drought or in arid climates.  They have been found to be toxic for all species of animals tested (Schoental, 1963), though some species, notably the guinea-pig, are resistant (Chesney & Allen, 1973a; White et al., 1973). 

    Human disease caused by Pyrrolizidine alkaloid toxicity has been known to be endemic in the central Asian republics of the USSR, at least since the early thirties (Ismailov, 1948a,b; Mnushkin, 1949) when several outbreaks occurred, and the cause was discovered to be the seeds of plants of  Heliotropium species (Dubrovinskii, 1947, 1952; Khanin, 1948), which contaminated the staple food crops. A spate of reports followed, mostly from the West Indies, of acute and chronic liver disease (Bras et al., 1954, 1961; Bras & Hill, 1956; Stirling et al., 1962), associated with the ingestion by people of herbal infusions for the treatment of certain ailments.  Schoental (1961) and Davidson (1963) suggested that, in view of the evidence of the hepatotoxicity of Pyrrolizidine alkaloids, consumption of plants containing them could be of etiological significance in human liver disease, especially in developing countries where they are consumed as food or herbal medicines. In spite of this, and the fact such an ubiquitous source of toxic material is capable of producing animal and human disease and that there have been more recent reports, the Pyrrolizidine alkaloids have not attracted much attention in the world as a health hazard.  In fact, a recent handbook on naturally occurring toxic agents in food (Rechicigl, Jr, 1983) refers to them only in passing and makes no mention of human disease caused by them. Veno-occlusive disease (VOD) (Bras & Hill, 1956), which is characterized by the dominant occlusive lesion of the centrilobular veins of the liver lobule and is caused by these alkaloids, has since been reported from all parts of the world, in both man and animals (Hill, 1960; Bras, 1973). It has been attributed to the accidental contamination of food by toxic plant products or the ingestion of herbal infusions. 

  5. Oxyuranus Microlepidotus

    Oxyuranus microlepidotus is the scientific name for Western Taipan, Inland Taipan,  Fierce Snake, and Small-scaled Snake. Oxyuranus microlepidotus or Taipans are a relatively minor cause of snakebites in Australia in relation to numbers of cases, but assume a far more important position due to the extreme hazard of their bites. Without appropriate antivenom treatment up to 75% of taipan bites will be fatal. Indeed, in the era prior to specific antivenom therapy, virtually no survivors of taipan bite were recorded. Main risks are neurotoxic paralysis, coagulopathy, rhabdomyolysis, acute renal failure. Target organs are neuromuscular junction, coagulation system, skeletal muscle.

    Local effects appear variable, not all cases being significantly painful. Bite marks from Oxyuranus microlepidotus are usually visible, due to the moderately large fangs, but in some cases local erythema or edema may be absent. A complete set of teeth marks including fangs, post-maxillary teeth, pterygopalatine teeth and mandibular teeth may be present. However, only minor fang marks may be seen in other cases. Local secondary infection is unusual. The venom from Oxyuranus microlepidotus may spread to draining lymph nodes with consequent pain and/or tenderness and/or swelling. Local symptoms and signs may be made worse by prolonged use of first aid.

    Symptoms include headache, nausea, vomiting, abdominal pain, impaired conscious state, occasionally (especially in children) loss of consciousness and convulsions.  Coagulopathy rarely occur with overt bleeding manifestations. Progressive neurotoxic paralysis, muscle movement pain and acute renal failure are also indications.

    Oxyuranus microlepidotus venom is used both in antivenom production and for laboratory research. The neurotoxins in particular have proved valuable neuromuscular transmission research, while the procoagulant has been used in assays of prothrombin level in plasma and other studies on blood coagulation.

    The rate and amount of absorption will depend on the quantity of Oxyuranus microlepidotus venom injected, the depth of injection, site of injection including vascularity, the activity of the victim, and the type, efficiency of application and length of application of first aid. Clinical evidence from human cases of envenomation suggests that much initial venom movement is via the lymphatic pathways.  This is supported by work in monkeys using RIA to detect whole venom.

    Initially the patient will usually be anxious, knowing they sustained a snake bite from Oxyuranus microlepidotus. The subsequent course will depend on (a) amount of venom injected, (b) size of patient relative to venom load (ie children may be worse affected), (c) degree of activity of patient after bite (physical activity hastens venom absorption), (d) timing, type, effectiveness of first aid, (e) speed and nature of specific medical treatment given, if systemic envenomation ensues, (f) pre-existing health factors for each patient (ie past renal problems, allergic problems etc).

  6. Pseudechis Australis

    Pseudechis australis (mulga snake, king brown) snakes are found in a diverse range of habitats from arid areas across central Australia, through to sub-tropical and tropical regions. Principally diurnal, it is however active on warm nights.

    Black snakes are only a moderately common cause of significant snakebites in Australia. Severity depends on species, with Pseudechis australis often causing significant envenomation while some other species, notably P. porphyriacus, only rarely causing severe envenomation. In the past P. papuanus has been thought to be a significant cause of snakebites in Papua New Guinea, but there is some doubt that this is still so.

    Main risks are rhabdomyolysis, acute renal failure, and possibly coagulopathy and neurotoxic paralysis in some species. Target organs are the skeletal muscle, coagulation system, and possibly the neuromuscular junction for some species.

    Locally, clinical effects usually immediately painful, with subsequent development of mild to marked local edema, and sometimes ecchymosis. Bite marks vary from single puncture, through multiple punctures, to multiple scratches. Local secondary infection unusual. Venom may spread to draining lymph nodes with consequent pain, tenderness or swelling.

    Systemic effects include headache, nausea, vomiting, abdominal pain, impaired consciousness, occasionally loss of consciousness and possibly convulsions. Coagulopathy with overt bleeding manifestations is rare. Neurotoxic paralysis is not well documented clinically. Muscle movement is painful. Acute renal failure. Rhabdomyolysis may dominate the clinical picture for Pseudechis australis bites and possibly for P. butleri bites.

    The human lethal dose for Pseudechis australis venoms is unknown. However, without antivenom treatment, a significant number of Pseudechis australis bites will prove fatal. The same may apply for P. papuanus and possibly  P. butleri (for which there are no human case reports), but for P. porphyriacus, and possibly P. colletti and P. guttatus human fatalities are very rare, and envenomation by these species is unlikely to be life threatening, except perhaps in a small child.

    Initially the patient will usually be anxious, knowing they have sustained a snakebite.  The subsequent course will depend on (a) amount of venom injected, (b) size of patient relative to venom load (ie children may be worse affected), (c) degree of activity of patient after bite (physical activity hastens venom absorption), (d) timing, type, effectiveness of first aid, (e) speed and nature of specific medical treatment given, if systemic envenomation ensues, (f) pre-existing health factors for each patient (ie past renal problems, allergic problems etc). Bites will vary in severity with the species of black snake involved in addition to the factors mentioned above.

  7. Bacillus Thuringiensis

    Commercial Bacillus thuringiensis (Bt) products are microbial pest control agents (MPCAs) containing specific insecticidal proteins (ICPs) and most often living spores as well as formulating agents. They are processed fermentation products. Bacillus thuringiensis is a facultative anaerobic, motile, gram-positive, spore-forming bacterium. The formation of parasporal crystals adjacent to the endospore during sporulation stages III to IV distinguishes Bacillus thuringiensis from other Bacillus species.

    Bacillus thuringiensis, like other Bacillus species, has been classified on the basis of its cellular, cultural, biochemical and genetic characteristics (Baumann et al., 1984; Claus & Berkley, 1986; Slepecky & Hemphill, 1992; Carlson & Kolsto, 1993; Hansen et al., 1998). In 1958, Heimpel & Angus (1958) introduced a classification scheme to identify these crystalliferous bacteria based on their morphological and biochemical characteristics. However recent molecular analysis shows that several variations can be found within serotypes, and that specific biochemical characteristics do not always refer to a specific serotype (Helgason et al., 1998; Hansen et al., 1998).

    Commercial Bacillus thuringiensis products do not contain metabolites that are considered hazardous to humans and the environment. However, Bacillus thuringiensis, like other bacteria, may produce during the vegetative growth and sporulation stages an assortment of antibiotics, enzymes, metabolites and toxins that are biologically active and may have effects on both target and non-target organisms (NTOs).

    Bacillus thuringiensis, like other members of the genus Bacillus, has the ability to form endospores that are resistant to inactivation by heat and desiccation and that persist in the environment under adverse conditions (Stahly et al., 1991). When considering the degradation of Bacillus thuringiensis in the environment, it is important to distinguish between changes in the numbers of viable spores and changes in biocidal activity. The survival and activity in the environment have been reviewed by Hansen et al. (1996).

    Bacillus thuringiensis may be lost to the soil by overspray during application or by the action of rain on plant surfaces. Further losses arise from in situ degradation by environmental factors, such as ultraviolet (UV) radiation and microbial activity (Griego & Spence, 1978; Sorenson & Falcon, 1980; Beegle et al., 1981; West et al., 1984a,b). Pedersen et al. (1995) found that Bacillus thuringiensis was dispersed by rain splash from the soil to the lower leaves of cabbage.

    Conventional Bacillus thuringiensis products, which utilize naturally occurring or modified Bacillus thuringiensis strains, account for approximately 90% of the world MPCA market (Bernhard & Utz, 1993). Current annual production of Bacillus thuringiensis has been estimated at 3000 or more tonnes in developed countries. In China, up to 10 000 tons are produced annually (personal communication by Guan Xiong, Fujian Agricultural, University, 1997).

  8. Domoic Acid

    Domoic acid was first isolated from the red alga Chondria armata. In 1975 it was identified as coming from the Mediterranean Alsidium corallinum It was later found in either microalgae species (diatoms) or macroalgae species (red algae) (IOC,1995). Bivalve molluscs are contaminated by filtering toxic dinoflagellates and accumulating the toxins in their digestive system. As for the crabs observed to contain domoic acid in Oregon, USA, the toxins concentrated mostly in the digestive system even if lower concentration could be found in the flesh. Dinoflagellate-eating fish may also become contaminated.

    Domoic acid is an excitatory amino acid containing the structure of glutamic acid and resembling kainic acid (Todd, 1989). Three geometric isomers of domoic acid have been described; they are isodomoic acids D, E, and F. They have little biological activity compared to domoic acid.

    Seaweed Chondria armata may contain domoic acid and extracts of the plant have been used in Japan as an ascaricidal medication at a dose of 20 mg per person without adverse effects (Daigo, 1959).  Its insecticidal properties were also known since flies die soon after landing on the seaweeds (Iverson, 1990).

    Amnesic shellfish poisoning (ASP) occurs after ingestion of bivalve mollusks or possibly fish contaminated with domoic acid. Gastro-intestinal symptoms may precede the neurological symptoms. These may be quite mild and the CNS may be the first target organ affected. Until now, only bivalve mollusks harvested in Prince Edward Island, Canada, have produced poisonings in humans. Domoic acid has been found in algae or dinoflagellates in Japan, the Mediterranean region, the East Coast of North and South America, and the West Coast of North America.

    After a delay of a few hours to one-day post ingestion of mollusks contaminated with domoic acid, gastrointestinal symptoms appear. They may include nausea, vomiting, abdominal cramps, diarrhea, hemorrhagic gastritis and anorexia. The neurological symptoms may occur after a delay of a few hours or up to three days according to the outbreak observed in 1987. These consist of a wide variety of symptoms varied among patients: severe headaches, loss of balance or dizziness, vision disturbances, memory loss. In more severe cases (old age and renal insufficiency being the two main risk factors): symptoms included confusion, disorientation, mutism for up to two weeks; autonomic nervous system dysfunction for a few days to a few weeks (cardiac arrhythmias, unstable blood pressure, hiccoughs, bronchial hypersecretions which may require endo-tracheal intubation); involuntary chewing, grimacing, myoclonia, convulsions; coma. Death occurred in 4 of the 107 confirmed cases. Permanent sequelae included memory loss and peripheral polyneuropathy.

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