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T-2 Toxin, A Trichothecene Mycotoxin
T-2 has been found in samples procured from water-damaged buildings. Fusarium spp. are the mold that usually makes T-2, although Myrothecium and Stachybotrys also make T-2, and in some samples it has been associated with other molds. Fusarium species shown to make T-2 are Fusarium moniliforme, F. equiseti, F. culmorum, F. solani, F. avenaceum, F. roseum, F. nivale Fusarium tricinctum, F. poae, F. sporotrichiella, F. graminearum.
Where You Might Come In Contact With The Trichothecene T-2
Food is where most people come in contact with this mycotoxin. Water-damaged buildings have also been found to contain T-2 toxin in the past. Studies looking at mycotoxins in water damaged-buildings have found it. In 1993, a high number of fatal pulmonary hemorrhages in infants originating from a small region of Ohio raised suspicion that the cause may have been due to trichothecene mycotoxin exposure in the homes secondary to mold overgrowth. Several cases of sudden infant death syndrome were also thought to be related to Stachybotrys mycotoxin exposure in homes secondary to mold overgrowth resulting from a flood. It is unusual for practitioners to consider mold exposure as the cause of health issues unless it slaps them in the face, so these cases had to be severe and fairly obvious.
Grains are where T-2 toxin is found the most often. T-2 toxin may contaminate small grains including wheat, corn, barley, rice, soybeans and particularly oats . T-2 is a problem in grain contamination in Europe, especially in the Nordic countries. In the 1940s in the Oregnburg District of the USSR, 10% of the population died from what they suspect was mass food poisoning from fusarium mold growing on grain that created T-2 toxin. T-2 toxin has been implicated as part of the alleged chemical warfare agent ‘yellow rain’ in Southeast Asia. Eyewitnesses claimed low flying aircraft released a yellow, oily liquid over Southeast Asian populations. T-2 is also claimed to be the cause of Gulf War Syndrome. (It would be nice if the classified documents around this scenario would be unclassified so people would know what the likely cause of their affliction is.)
Additionally animal products from animals who eat grain with T-2 contamination may be tainted with T-2 or one of 20 different metabolites of T-2. Farm animals are all to often fed moldy grain and hay.
As with other mycotoxins, indirect exposure from contaminated objects, and surfaces that are not property decontaminated has been shown to spread T-2 to other individuals.
Health Effects of T-2
T-2 toxin is known to be one of the most toxic trichothecene mycotoxins. In animal studies, toxicity is dependent on route of administration, the time and amount of exposure, the dosage administered, and the age, sex and overall health of the animal along with presence of any other mycotoxin. T-2 has been shown to penetrate the lungs easily as well as be topically absorbed, and has been shown to cause rapid response to skin contact and ingestion. T-2 is the only trichothecene that is known to be easily absorbed through the skin. T-2 is the most toxic when absorbed through the lungs. In addition to being highly toxic by itself, it also exacerbates the effect of ionizing radiation. The mechanism of action mainly consists of the inhibition of protein synthesis, and oxidative damage to cells followed by the disruption of nucleic acid synthesis and ensuing apoptosis.
T-2 toxin causes a fatal disease of humans known as alimentary toxic aleukia (ATA); a disease that was particularly problematic in Russia in the 1940s during the fusarium mold outbreak on their grains. The T-2 toxin also produces a similar ATA disease in cats.
There Are 4 Stages Of symptoms In ATA
1) Inflammation of the gastrointestinal tract - ulceration of mouth mucosa and gastrointestinal inflammation
2) Leukopenia (low white blood cells) and progressive lymphocytosis (increased number of lymphocytes - a type of white blood cells)
3) Skin symptoms, red rash, bleeding of the skin and mucous membranes may occur, which can cause strangulation and death.
4) Red blood cells and white blood cells are depleted, and the immune system is unable to respond. Infection can cause death.
A similar disease has been reported with trichothecene contaminated grains in Japan called Akakabibyo or red mold disease. Multiple countries, have had trouble with trichothecene poisoning of grains, including with T-2.
There is also a disease called "stachybotryotoxicosis" which was coined in the 1940s and was seen in horses first, but subsequently in other animals. It caused fever, listlessness, oral lesions, pancytopenia, hemorrhage, opportunistic infections and a high death rate.
Stachyboytris has been found in soil and materials rich in cellulose (hay, straw, grain, hemp, plant debris, dead roots, wood pulp, cotton, fabrics, paper, book bindery glue, plant fiber-processing plants,cigarette tobacco and cellulose based building materials
Blood Brain Barrier Permeability And Brain Toxicity
There has been many reports from research studies showing T-2 toxin appears to cross the blood brain barrier (BBB) and cause toxic effects on the central nervous system
- Changes in levels of brain monoamines in certain areas of the rat brain after T-2 toxin application have been described
- Oral administration of T-2 toxin in rats resulted in reduced motor activity and performance in a passive avoidance test
- Oxidative damage in brain of mice after dermal and subcutaneous exposure to T-2 toxin
- Gel zymograph was used to show T-2 induced alteration in BBB permeability is mediated through oxidative stress, activation of MMP-9, and proinflammatory cytokines in brain as well as contribution from peripheral tissue spleen.
- In vitro study showed BBB disruption with T-2 and HT-2 (main metabolite and showed less effect). Both were able to cross the BBB.
Quick Half Life
When consumed by animals, T-2 toxin is readily absorbed, metabolized and nearly entirely excreted within 48 hours and it is distributed through-out the body without affinity for any specific organ. In rodents it peaks after 30 minutes. In one study it's half-life was less than 20 inutes in plasma. The symptom onset is within minutes to hours.
Signs And Symptoms Of T-2 Toxin In Humans
- Severe itching, pain and redness of the skin, sores, necrosis and shedding of the skin
- Ulceration in the mouth
- Abdominal pain, with nausea, vomiting and diarrhea, anorexia
- Nose and throat pain, discharge from the nose, itching and sneezing
- Cough, difficulty breathing, wheezing, chest pain and spitting up blood
- Tachycardia (fast heart beat), vascular collapse if severe
- Distortion of any of the senses, dizziness, loss of the ability to coordinate muscle movement, hypotension, hypothermia
- Elevated body temperature, chills
- Complete degeneration of bone marrow
- Weeks after exposure: transient lymphocytosis, followed by bone marrow suppression with leukopenia, granulocytopenia and throbocytopenia. (results in temporary bleeding disorders - breakdown of red blood cells, ultimately reduced white blood cells)
- Death - due to opportunistic infections largely
Additionaly symptoms noted with T-2 toxicity are abortion, inhibition of protein synthesis, and allograft rejection.
Broiler chickens fed low doses of T-2 toxin may demonstrate symptoms of weight loss, feather malformation, and yellowing of the beak and legs.
T2 is produced predominantly by Fusarium sporotrichioïdes and F. langsethiae. Exposure to T-2 toxin is associated with low white blood cell counts and cell depletion in lymphoid organs as well as inhibition of red blood cell formation in bone marrow and the spleen. Furthermore, T-2 toxin reduces proliferation of the white blood cells called lymphocytes and it disturbs the maturation process of dendritic cells (an antigen presenting cell).
After hearing all these various ways that T2 depresses the immune system, it is no surprise that exposure to T-2 suppresses immune response to systemic bacterial infections such as Salmonella typhimurium, Listeria monocytogenes, Mycobacterium bovis, and Babesia microti. Respiratory immune defences are also compromised by T-2 exposure. T2 also has been shown to decrease viral resistance. If you have read much research on mycotoxins, you will already know that immunotoxicity is common amongst mycotoxins.
The acute affect of T-2 on rabbits was gastroenteritis, damage of digestive cells, liver cells, and white blood cells as well as adrenal cortex cells and the blone marrow. The subacute affect on rabbits was stomach inflammation, emaciation, and hypertrophy of the adrenal cortex.
The effects of T-2 mycotoxin poisoning will depend on the concentration of exposure, length of time and way the person is exposed.
Subacute affect of T-2 on rabbits displayed inflammation of the stomach lining, hypertrophy and emaciation of the adrenal cortex.
The chronic affect in animals seems to involve loss of weight, decreased red blood cell and white blood cell counts, decreased glucose levels and detrimental changes to the digestive tract. It has also been noted that it increases the infection rate of animals.
T-2 has been shown to inhibit protein synthesis, interfere with metabolism of membrane phospholipids and increases liver and brain LPO. It also suppresses glutathione-S-tranferase, increases reactive oxygen species generation, and depletes glutathione.
In rat research, T-2 elevated barin concentrations of tryptophan and serotonin, leading to an upsurge of dopamine. As the concentration of dopamine increased in the brain, the epinephrine levels decreased in the adrenals. The increased indolemine levels in the brain caused the animals to refuse food.
Possible Lab Value Changes
Lowered IL-2 and IL-5 production by T cells
Lowered dendritic cells
STILL WORKING ON THIS ARTICLE - Not Yet finished.
Mechanism Of Action
Oxidative Damage to lipids, proteins and nucleic acids Cause
- Mitochondrial dysruption
- Protein and DNA synthesis inhibition
- Reduces lymphocytes
- Alters membrane function
- Impairs production of antibodies
- Alters development of dendritic cells
- Causes Apoptosis of various cell types in vitro (shown in vivo in mice)
The main reactive oxygen species involved in the oxidation of proteins, lipids and DNA appear to be hydrogen peroxide, hydroxyl radical and superoxide molecules. The mitochondrial complex I and CYP450 have also been reported to be involved in mycotoxin-induced ROS generation.
T-2 toxin is also known to decrease function of the innate immune system. T-2 toxin is thought by researchers to bind and inactivate peptidyl-transferase activity at the transcription site, resulting in the inhibition of protein synthesis. This inhibitory effect is most notable in actively proliferating cells, such as the skin and gastrointestinal tract, the bone marrow and thyroid, and erythroid cells. It is thought that the T-2 toxin disrupts DNA polymerases, terminal deoxynucleotidyl transferase, monoamine oxidase and several other proteins involved in the coagulation pathway.
Trichothecenes are known to interact with subcellular structures, resulting in the disruption of the mitochondrial form and structure, rough endoplasmic reticulum and other membranes. Trichothecenes decrease the activity of metabolically critical enzymes such as succinic dehydrogenase, decreasing the oxidation of succinate, malate and pyruvate molecules and additionally inhibiting protein synthesis in mitochondria. The oxidative stress due to the T-2 toxin in rat liver cells can be reduced using l-carnitine. Additionally low doses of T2 toxin in rats inhibits steroidogenesis by suppressing cAMP-PKA pathway, suggesting T-2 toxin has an endocrine disruptive effect.
Possible Treatments For T-2 Exposure
Chemically, the T-2 toxin has a positive charge and is insoluble in water but soluble in acetone, ethyl acetate, chloroform, ethanol, methanol and propylene glycol. Inactivation is said to be achieved by heating it to 900°F for 10 min or 500°F for 30 min. There are bacteria and fungi that can also inactivate it by altering its chemical structure.
People who live in areas with trichothecene produced by fusarium and have sensitivity to trichothecenes, feel like air filters can help remove it from the air, and that below-freezing temperatures as well as snow may decrease its presence in the air. Although there are no studies on this that I know of, getting first hand information from people like this is very useful.
The military has had experience with T-2 and has put out some data on how to deal with exposure. They have a cream they use (Reactive Skin Decontamination Lotion ), which is not shared with you or me as it is considered a national secret. Here is what has been shared with the medical community: Remove all clothing, and clean and scrub the patient's entire skin surface with soap and water. Washing the contaminated area of the skin within 6 hours post exposure can remove 80-98% of the toxin and has been demonstrated to prevent skin lesions and death in experimental animals.(This is true with other mycotoxins often too and is why sensitive people should always wash their body, hair, wash eyes (remove contacts and put them with the contaminated clothing. Do not put the contacts back in your eyes again.) if irritated and gargle as well as rinse their nose after exposure. It can help people who are really sensitive to mycotoxins in general.) They claim the proposed mechanism of action is neutralization of traditional chemical warfare agents by a combination of physical removal and nucleophilic breakdown, which renders the original toxic substance nontoxic. It is suggested that clothing be contained and disposed of. (Clothing of sensitive people who are exposed to usual mycotoxins in water-damaged buildings should always be washed and I suggest with a good hydrogen peroxide bleach. However, their suggestion to throw away contaminated clothing after bagging it carefully is a good idea in some cases of mycotoxin exposure and certainly would be if caught in "yellow rain". )
The T-2 toxin is able to undergo microbial transformation into its deepoxylated form in the intestine which is very important in toxic-reducing pathway.
It has been found that selenium can partly block chondrocyte apoptosis induced by the T-2 toxin by reducing the Bax/Bcl-2 ratio.
Biotransformation Of T-2 Toxin
Rumninants are thought to be somewhat resistant to T-2 toxin in comparison with monogastric animals. It is thought to be due to their ability to de-epoxidate deacetylate the toxin in their rumen. Their gut bacteria appear to be protecting them by altering the mycotoxin. They are still affected by T-2, but it is more subdued. T-2 in dairy cattle is associated with feed refusal, production losses, gastroenteritis lesions, intestinal hemorrhages and death but not as much as in non-ruminant animals.
Dietary Substances that help minimize toxicity of T-2
Substances that have been shown to help alleviate T-2 toxin Damge
- Amino acids
Antioxidants That Are Thought To Be Beneficial
- Vitamin E
- Chlorophyll and its derivatives, Phenol rich plants/herbs
- Selenium - sodium selenite in mice prevented erythrocyte membrane damage induced by T-2 toxin
- N-Acetyl-cysteine (NAC) protects chicken growth plate chondrocytes from T-2 toxin-induced oxidative stress
Research with rats showed some benefit from use of bentonite clay although the research was not set up the way I would have done it. In one study it was given at the same time as the T-2 toxin while in another it was given prior to the T-2 toxin. Since there were some positive outcomes in the studies, I think more research would be called for that is set up better.
STILL WORKING ON THIS ARTICLE - Not Yet finished.
Quercetin - Reduced T-2 induced apoptosis in rabbits
Used as an antioxidant in cases of T-2 toxicity in the liver of rats, as it aided in decreasing TBAR-induced lipid peroxidation, SOD, GST, total lipids and elevated total thiol and catalase levels as well as hemoglobin and hematocrit values
Shown to protect liver against T-2 toxin by reducing lipid peroxidation and modulating GSH metabolism in chicks.
In poultry Hippophae rhamnoides (sea buckthorn) alone protected the immunosuppressant action of the T-2 toxin, but sea buckthorn and glucomannan in combination provided a synergistic effect with regard to protection against T-2 toxicity
mucilage from quince seeds is a potential treatment of T-2-toxin-induced dermal injuries in rabbit. Quince seed mucilage (15% in cream) has more and better healing effects on dermal toxicity caused by T-2 toxin comparing to no treatment or eucerin cream without mucilage.
Exposure to sodium hypochlorite can destroy the toxic activity of the toxin according to a medline article.
Glucomannans Used For T-2 Toxicity
Chickens given T-2 were partially protected by glucomannans: The partial protective effect of the glucommanans on the antioxidant defences in the chicken liver were as follows: The selenium concentration in the liver was restored completely, although the selenium-glutalthione-peroxidase activity in the liver increased to only 81% of its control value. These protective effects of modified glucomannans were associated with a 45% reduction of lipid peroxidation in the liver in comparison to the effects of T-2 toxin alone. A combination of modified glucomannans with organic Se was shown to provide further protection against toxin-induced antioxidant depletion and lipid peroxidation in the chicken liver. See the research below.
Ongoing Research And Future Thoughts
Detoxification genes are being studied to clone them and express them in microorganisms to develop recombinant microorganisms that are biologically and ethically appropriate for industrial-scale enzyme production and purification. The development of host resistance strategies can also be employed to realize effective methods which target T-2 toxin decontamination by the biotransformation system.
Toxicol Sci. 2008; 104(1):4-26 (ISSN: 1096-0929)
Stachybotrys chartarum, trichothecene mycotoxins, and damp building-related illness: new insights into a public health enigma.
Pestka JJ; Yike I; Dearborn DG; Ward MD; Harkema JR
Damp building-related illnesses (DBRI) include a myriad of respiratory, immunologic, and neurologic symptoms that are sometimes etiologically linked to aberrant indoor growth of the toxic black mold, Stachybotrys chartarum. Although supportive evidence for such linkages is limited, there are exciting new findings about this enigmatic organism relative to its environmental dissemination, novel bioactive components, unique cellular targets, and molecular mechanisms of action which provide insight into the S. chartarum's potential to evoke allergic sensitization, inflammation, and cytotoxicity in the upper and lower respiratory tracts. Macrocyclic trichothecene mycotoxins, produced by one chemotype of this fungus, are potent translational inhibitors and stress kinase activators that appear to be a critical underlying cause for a number of adverse effects. Notably, these toxins form covalent protein adducts in vitro and in vivo and, furthermore, cause neurotoxicity and inflammation in the nose and brain of the mouse. A second S. chartarum chemotype has recently been shown to produce atranones-mycotoxins that can induce pulmonary inflammation. Other biologically active products of this fungus that might contribute to pathophysiologic effects include proteinases, hemolysins, beta-glucan, and spirocyclic drimanes. Solving the enigma of whether Stachybotrys inhalation indeed contributes to DBRI will require studies of the pathophysiologic effects of low dose chronic exposure to well-characterized, standardized preparations of S. chartarum spores and mycelial fragments, and, coexposures with other environmental cofactors. Such studies must be linked to improved assessments of human exposure to this fungus and its bioactive constituents in indoor air using both state-of-the-art sampling/analytical methods and relevant biomarkers.
Int J Environ Res Public Health. 2013 Jul 9;10(7):2834-44. doi: 10.3390/ijerph10072834.
Protective effects of sodium selenite against aflatoxin B1-induced oxidative stress and apoptosis in broiler spleen.
Wang F1, Shu G, Peng X, Fang J, Chen K, Cui H, Chen Z, Zuo Z, Deng J, Geng Y, Lai W.
The aim of this study was to investigate the possible protective role of sodium selenite on aflatoxin B1-induced oxidative stress and apoptosis in spleen of broilers. Two hundred one-day-old male broilers, divided into five groups, were fed with basal diet (control group), 0.3 mg/kg AFB1 (AFB1 group), 0.3 mg/kg AFB1 + 0.2 mg/kg Se (+Se group I), 0.3 mg/kg AFB1 + 0.4 mg/kg Se (+Se group II) and 0.3 mg/kg AFB1 + 0.6 mg/kg Se (+Se group III), respectively. According to biochemical assays, AFB1 significantly decreased the activities of glutathione peroxidase, total superoxide dismutase, glutathione reductase, catalase and the level of glutathione hormone, while it increased the level of malondialdehyde. Moreover, AFB1 increased the percentage of apoptosis cells by flow cytometry and the occurrence of apoptotic cells by TUNEL assay. Simultaneous supplementation with sodium selenite restored these parameters to be close to those in control group. In conclusion, sodium selenite exhibited protective effects on AFB1-induced splenic toxicity in broilers by inhibiting oxidative stress and excessive apoptosis.
[Indexed for MEDLINE]
Free PMC Article
Comp Biochem Physiol C Toxicol Pharmacol. 2007 May;145(4):582-7. Epub 2007 Feb 12.
Protective effect of modified glucomannans and organic selenium against antioxidant depletion in the chicken liver due to T-2 toxin-contaminated feed consumption.
Dvorska JE1, Pappas AC, Karadas F, Speake BK, Surai PF.
The aim of this work was to assess the effect of T-2 toxin on the antioxidant status of the chicken and to study possible protective effects of modified glucomannan (Mycosorb) and organic selenium (Sel-Plex). Inclusion of T-2 toxin in the chickens' diet (8.1 mg/kg for 21 days) was associated with significant decreases in the concentrations of selenium (Se)(by 32.2%), alpha-tocopherol (by 41.4%), total carotenoids (by 56.5%), ascorbic acid (by 43.5%) and reduced glutathione (by 56.3%) in the liver, as well as a decrease in the hepatic activity of Se-dependent glutathione peroxidase (Se-GSH-Px) (by 36.8%). However, inclusion of modified glucomannans into the T-2 toxin-contaminated diet provided a partial protection against the detrimental effects of the mycotoxin on the antioxidant defences in the chicken liver. For example, the Se concentration in the liver was restored completely, although the Se-GSH-Px activity in the liver increased to only 81% of its control value. These protective effects of modified glucomannas were associated with a 45% reduction of lipid peroxidation in the liver in comparison to the effects of T-2 toxin alone. A combination of modified glucomannas with organic Se was shown to provide further protection against toxin-induced antioxidant depletion and lipid peroxidation in the chicken liver. Thus, the data clearly indicate a major protective effect of the mycotoxin-binder in combination with organic Se against the detrimental consequences of T-2 toxin-contaminated feed consumption by growing chickens.
[Indexed for MEDLINE]
Poult Sci. 1997 Sep;76(9):1205-11.
Edrington TS1, Kubena LF, Harvey RB, Rottinghaus GE.
To evaluate the effectiveness of a superactivated charcoal (SAC) in alleviating mycotoxicosis, two experiments were conducted in which 432 male broiler chicks (216 per experiment) were fed diets containing 4 mg aflatoxin (AF) or 6 mg T-2 toxin/kg of diet, with and without 0.5% SAC, from 1 to 21 d of age. Feeding AF and T-2 toxin significantly decreased BW gain over the 21-d experimental period. Inclusion of SAC in the diet containing AF resulted in BW gains that were intermediate between gains of chicks fed AF and those of controls. No benefits were seen in BW gain when SAC + T-2 toxin was fed. Feeding AF increased relative weights of liver, spleen, and kidney; however, only liver weight in Experiment 1 was similar to controls when SAC was included. Of the blood parameters altered by AF (decreased cholesterol, inorganic phosphorus, total protein, and urea nitrogen, and increased mean corpuscular volume and hematocrit in Experiment 1; decreased albumin and total protein, and increased creatine kinase in Experiment 2) only urea nitrogen, hematocrit, and inorganic phosphorus (Experiment 1) and hematocrit (Experiment 2) were comparable to controls when SAC was included in the diet. Feeding T-2 toxin decreased serum cholesterol, total protein, urea nitrogen, and mean corpuscular volume; however, only cholesterol and mean corpuscular volume were improved with the addition of SAC (Experiment 1). Oral lesions were observed in birds fed T-2 toxin with no difference in severity when SAC was added in Experiment 1, however in Experiment 2, birds fed SAC + T-2 had a significantly lower lesion scores than those fed T-2 alone. Mortality was noted in both experiments but was not influenced by SAC treatment. These findings suggest that the addition of dietary SAC is marginally effective in alleviating some of the toxic affects associated with AF, but was of little benefit when T-2 toxin was fed to growing broiler chicks.
Food Chem Toxicol. 2016 Jan;87:128-37. doi: 10.1016/j.fct.2015.12.003. Epub 2015 Dec 10.
Toxicity and oxidative stress induced by T-2 toxin and HT-2 toxin in broilers and broiler hepatocytes.
Yang L1, Yu Z2, Hou J3, Deng Y1, Zhou Z1, Zhao Z1, Cui J1.
T-2 and HT-2 toxins belong to mycotoxins which are found in human foods and animal chow. We investigated the toxicity and oxidative stress induced by T-2/HT-2 in broilers and chicken hepatocytes. Maize cultures of Fusarium poae was fed to broilers for 42 d, and the physiological index, biochemical index and expression of mRNAs related to oxidative stress were analyzed. Chicken hepatocytes were treated with different levels of T-2/HT-2, and the following parameters were detected: cell viability, GSH and MDA concentration, LDH leakage, activities of ALT/AST, ROS, GSH-PX, SOD and CAT, and expression of mRNA related to oxidative stress. In vivo, high levels of mycotoxins (4 mg/kg T-2 and 0.667 mg/kg HT-2) in feed caused significant reductions in body weight, weight gain, and serum total protein, and significant increases in feed conversion ratio, ALP, ALT/AST activities, and expression of mRNA related to oxidative stress. In vitro, cells treated with T-2/HT-2 showed reductions of GSH concentration and significant increases in LDH leakage, ALT/AST ROS, GSH-PX, SOD and CAT activities, MDA concentration, and expression of mRNA related to oxidative stress. Consequently, F. poae culture material and T-2/HT-2 induced toxicity and oxidative stress in vivo and in vitro, respectively.
Copyright © 2015 Elsevier Ltd. All rights reserved.
Broilers; Hepatocytes; Oxidative stress; T-2 and HT-2 toxin; Toxicity
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