Toxins are called toxins because they are toxic! This may sound obvious and patronising, but it must be clearly stated. To be nonchalant about the level of toxins in one's body is unwise. There is no good reason to insist on keeping all the toxins absorbed over time, whilst accumulating more and more with age. They are not our friends or desirable or pleasurable. They should not be there and cause huge damage to our biochemical functioning. If you care about your car, you would not leave dirty and old oil in the engine would you? How much more should you have 'clean mechanicals' inside your body!
Harmful phases of toxins tend to be fat soluble (lipophilic) and attach themselves to the lipid compartments (fat/lipid molecules) in the body. They are hard to remove from these places and are also difficult to transport across cell membranes for excretion. Toxins that are not effectively cleared from the body by the liver and kidneys thus end up usually in two places:
In the fat cells and fatty tissues of the body, including the brain, where they cause the minimum of harm (in relative terms). This is the body's mechanism for 'safely' storing/hiding toxins. Please see Wikipedia's definition of fat cells.
Attached to the inter- and intra-celllular membranes where they cause a huge amount of harm and prevent the effective and efficient exchange of nutrients and the body's biochemical compounds (resulting in impaired biochemical functioning, a decline in cellular membrane health and nutritional deficiencies (even if nutrient levels ingested are very high)). The presence of unwanted substances that can interfere with mitochondrial function (e.g. heavy metals, PCBs, toxic organic compounds and partial detoxification products like glutathione conjugates and peptide complexes (e.g. the body's detoxification molecule bondeds with a toxic organic chemical compound or a drug like antiobiotics) contribute to a condition known as Neurotoxic Membrane Syndrome.
An article 'The Detoxx System: Detoxification of Biotoxins in Chronic Neurotoxic Syndrome' [a.k.a. Neurotoxic Membrane Syndrome] by John Foster, M.D., Patricia Kane, Ph.D., Neal Speight, M.D. is shown at the link below.
A toxified body is unlikely to function optimally and the affected person will not naturally feel as good as he would otherwise (not jumping out of bed every morning!) This is partly on account of mitochondrial inefficiency and the compromising of the mitochondrial membranes with toxins and partial detoxification products, but also the displacement effect that toxic metals also have on the essential minerals in our bodies.
The immune system is particularly affected. It is clear that we are born with a certain amount of toxins from our mothers but accumulate more and more over time during our lives. Detoxifying the body is likely to help to balance the immune system in those with auto-immune system disorders and to enhance the immune system of those with an impaired immune system. It is also likely to aid in weight loss, as the fats that are required by the body to bind with toxins are no longer required.
People may associate obese or overweight people with toxins, and slim, skinny people with being clean and toxin free. Whilst various types of toxins attach themselves most readily to fatty tissues in the body, the slender, athletic person still has plenty of fatty tissues and cell membranes for toxins to attach themselves to. So the body type is not so important as far as a toxicity perspective goes. However, which body type is easiest to detoxify is another matter.
Every person's body reacts differently to toxicity. Establishing in absolute terms the levels of heavy metals in a person's tissues or blood is only so useful, as a 'low' level may have a negligible effect in one person and a huge debilitating effect in another. The reaction to a particular toxin is dependent in part to the individual's immune system's response to the presence of that particular level of that particular chemical in the blood stream. The definitions of what constitutes 'low' and 'significant' levels vary from agency to specialist. In reality, no level of toxicity is a good thing. If you can 'get away' with something, that doesn't mean you should necessarily ignore it. It is good practice to avoid ingesting/taking in toxins if possible, and to help the body eliminate those we have accumulated, not only those that interfere with the body's core processes, but also those that by default cause oxidative damages to our cells and premature ageing, and those that are carcinogenic and may cause various forms of cancer in later life.
For a sufferer of CFS or related conditions, the effects of toxicity on an already poorly functioning biochemistry can be very significant indeed. I would suggest that every person suffering from CFS or related conditions should rule toxicity out of the equation of their health problems, and the only way to actually to do that with 100% certainty is to perform a full bodily detoxification programme. In the normal course of treatment, this is performed after harmful micro-organisms have been eliminated from the body. With the presence of large numbers of harmful micro-organisms, heavy metals and biotoxins, the body is unlikely to recover, even when all the other root causes are being effectively targetted.
Please see the Introduction section on the Liver Function page regarding the effect of toxins on the body and in particular toxin accumulation and liver function.
Please see below a list of chemicals (including pesticides, domestic products, foreign hormones and industrial chemicals) that are classified as 'Endocrine Disrupting Chemicals'. These then have a negative disruptive effect on the body's endocrine system glands and disrupt the normal hormonal functioning of the body, by either mimicking or inhibiting the body's hormones. Hormones are the regulatory chemicals in the body. In some animals, such as frogs, birds, fish and molluscs, they have produced infertility and gender changes. For more information on the Endocrine system, and Endocrine system imbalance, please see the a href="adrenal.html">Hormonal page.
Quoting from the 2007 paper 'Integrative Medicine and the Role of Modified Citrus Pectin/Alginates in Heavy Metal Chelation and Detoxification: Five Case Reports' by Isaac Eliaz, Elaine Weil and Barry Wilk:
'Heavy or toxic metals are stable trace elements which cannot be metabolized by the body and bio-accumulate in soft tissues (and bone), passing up the food chain to humans. These toxins are an integral by-product of industrial society and are unavoidable in our modern-day life. These include: mercury, lead, nickel, arsenic, cadmium, aluminum, platinum, the metallic form of copper, and others. These heavy metals have no function in the body and can be highly toxic, negatively influencing the body's metabolic processes, and impairing multiple physiological systems throughout the body. Toxic metal burden can induce impairment and dysfunction in the cardiovascular, gastrointestinal, immune, reproductive, urinary, endocrine, central and peripheral nervous systems, detoxification (colon, liver, kidneys, skin), energy production and enzy-matic pathways. Toxic heavy metals can negatively affect energy levels, memory, circulation, blood pressure, and cholesterol and triglyceride levels. If unrecognized or inappropriately treated, toxicity can result in significant illness, reduced quality of life, and possibly death. Symptoms of chronic exposure are very similar to symptoms of other medical conditions, and often develop slowly over months or even years, so their cause can be easily missed. Heavy metal toxicity is a significant global health issue that can cause health problems of varying degrees in multiple systems. The two most common heavy metals that cause adverse effects are mercury and lead. Addressing heavy metals as part of an integrative medical plan can aid in the prevention and treatment of multiple ailments.'
Heavy metals bind to Krebs Cycle enzymes, involved in Mitochondrial Function and can also upregulate the body's immune system response, which in turn can result in more cellular inflammation, increased immune system free radical activity and an impetus for increased Nitric Oxide production.
One of the harmful effects of heavy metal toxicity is enzyme and protein inhibition, for example zinc finger proteins (the Cysteine-based Metallothionein family). A zinc finger is defined as finger-shaped fold in a protein that permits it to interact with RNA and DNA. The fold is created by the binding of specific amino acids in the protein to a zinc atom. Zinc-finger proteins function is to regulate the expression of genes (cellular division) as well as nucleic acid recognition, reverse transcription and virus assembly. The zinc finger proteins are thus proteins stabilised by a zinc atom. Without the zinc atom present, the protein will not function properly. The zinc atom in zinc finger proteins are often displaced by a heavy metal atom, for example arsenic or mercury. By removing the offending heavy metal atoms, the zinc atoms can be reabsorbed and assimilated into the zinc finger proteins, allowing the immune system to function normally (and accurately).
Porphyrins are the conjugate acids of ligands that bind with +2 or +3 metal ions to form complexes. Porphyrins are intermediary compounds in the production of Heme, and the respective enzymes involved with converting one form of Porphyrin to another are particularly sensitive to the presence of heavy metals or certain organic chemical toxins. Presence of these foreign toxins can inhibit the enzymes involved in these intemediary steps, thereby resulting in elevated levels of these intermediary products in the urine; and consequently too little Heme being produced.
A simple type of Porphyrin has the characteristic hole in the centre which can accommodate a metal ion.
Heme is a type of porphyrin-based protein, which contains an Iron atom at the centre of a large heterocyclic organic ring called a porphyrin. Not all porphyrins contain iron, but a significant proportion of porphyrin-containing metalloproteins have Heme as their prosthetic group. These are known as Hemoproteins (or Heme-containing proteins).
There are 3 main types of Heme in the body, Heme A, B and C. Heme B is the most common.
Heme also has many other functions such as electron transfer and catalysis (reaction rate control). Probably the three most important applications of Heme B in the human body however are in the Hemoglobin (a.k.a. Haemoglobin), Myoglobin and Peroxidase Family Enzymes.
Hemoglobin - is the pigment in Red Blood Cells that is used to bind with Oxygen and carry it from the lungs to the capillaries, where the O2 is squeezed out. The Hemoglobin molecule contains 4 Hemes.
Myoglobin - is the primary oxygen-carrying (storage) pigment of muscle tissues, and its oxygen binding abilities are unaffected by oxygen pressure. Myoglobins give meat its red colour. Myoglobins are the primary form of storage of oxygen in muscle cells, and are a secondary source of oxygen besides the primary source from the blood in the capillaries.
Peroxidase - is a large family of enzymes. Various types of Hemes are involved in the formation of certain Cytochrome enzymes. Three significant examples are:
Cytochrome c Oxidase (a.k.a. Complex IV) is the last enzyme involved in the electron transport chain of mitochondria, located in the mitochondrial membrane. It is involved with the synthesis of ATP. It is partially deactivated by displacement of the Copper centres by a heavy metal such as Mercury.
Cytochrome c Peroxidase (CCP). CCP is a water soluble heme-containing Peroxidase enzyme that reduces hydrogen peroxide to water. It is found in the inner membrane of the mitochondrion, and helps prevent oxidative damage to the mitochondrial membrane during respiration.
Cytochrome P450 - are a category of Liver enzyme involved in Phase I Regulation in the liver, in a variety of processes for treating waste products and toxins in the blood. Please see the Phase I and II Liver Pathways section above.
Clearly if heavy metal toxicity has impacted the Porphyrin conversion and Heme metabolism pathway, then there could be a serious impact on Hemoglobin levels in the red blood cells in the blood stream and Oxygen transport in the body.
As the Porphyrin pathway is particularly sensitive to toxicity (heavy metal ions binding with them and preventing them from being converted in the Porphyrin/Heme pathway), it is a particularly good indicator of toxicity. In other words, the Urinary Porphyrins can provide us with information about the extent of heavy metal toxicity in the body and the extent to which it is interfering with normal bodily biochemical processes. It thus differs from a urine test or blood test for heavy metal levels as it provides us with direct information about the problems the current heavy metal levels are causing in the body, which is arguably what is really important.
The levels of the following Porphyrins are measured.
Uroporphyrins I & III (a.k.a. uP)
Heptacarboxyporphyrin (a.k.a. 7-Carboxyporphyrin, 7cxP or 7cP)
Hexacarboxyporphyrin (a.k.a. 6-Carboxyporphyrin, 6cxP or 6cP)
Pentacarboxyporphyrin (a.k.a. 5-Carboxyporphyrin, 5cxP or 5cP)
Precoproporphyrin (a.k.a. PrCP or pcP)
Coproporphyrins I & III (a.k.a. cP)
The absolute levels and also the relative ratios of the different Porphyrins in the urine can provide us with information about what kind of heavy metal is causing the problem in the Heme biosynthesis pathway, and thus assist in the determination of chelation strategy.
Interpretive examples of the absolute values are listed below.
High uP = Aluminium (Al) toxicity
High uP and 7cP = Arsenic (As) and certain organic chemicals (e.g. Polychlorinated Biphenyl (PCB)) toxicity
High 6cP, 5cP and cP = Mercury (Hg) and certain organic chemicals toxicity
High 5cP, pcP and cP = Hg Toxicity
High pcP and cP = Hg Toxicity
High cP = Lead (Pb) Toxicity
Interpretive examples of the relative ratios are listed below.
High pcP/uP = uP is unresponsive to Hg toxicity hence this ratio is an indicator of Hg toxicity
High pcP/cP = assuming pcP is elevated, this ratio is a marker for Hg toxicity, partially modulated by genetic factors
High (5cP+pcP)/(uP+7cP) = highlights the Hg specific Uroporphyringoen Decarboxylase (URO-D) gene, site 4, relative to other active gene sites - therefore an indicator of Hg Toxicity
High cP/uP = Pb Toxicity
Low cP/uP = Xenobiotics (misc. pollutants, often organic) Toxicity
On the condition that PrcP i increased, the ratio PrcP/cP may constitute a marker of heavy metal toxicity (mercury), partly modulated by genetic factors (i.e. hereditary Porphyria). The above ratios are devised to largely eliminate genetic factors from the measurement of indirect heavy metal toxicity.
Herditary Porphyria is a group of inherited disorders of certain enzymes involved in this Heme biosynthetic pathway, called the Porphyrin pathway. They come in the form Acute Porphyria or Cutaneous Porphyria. Acute porphyria mainly affects the nervous system and can manifest itself in spikes, where the Porphyrin levels can become so high that many severe symptoms such as abdominal pains, vomiting, acute neuropathy, muscle weakness and mental disturbances are experienced. Enzyme injections are required during such spikes. It can even result in death if not handled correctly. Cutaneous Porphyria mainly affects the skin and results in photosensitivity, blisters, necrosis of the skin and gums, itching, swelling and hair growth on the forehead.
As stated in the link below, the accumulation of porphyrins can be problematic as they are toxic if present in high enough concentrations. In the case of heavy metal toxicity induced porphyria, it is unlikely that the levels will rise as much as they do in hereditary porphyria, and constitute significant toxicity on the body. The toxicity effect of the heavy metals in the body that are producing these somewhat elevated levels of porphyrins are far more likely to be constituting a serious toxicity effect on the body.
'Deficiency in the enzymes of the porphyrin pathway leads to insufficient production of heme. Heme function plays a central role in cellular metabolism. This is not the main problem in the porphyrias; most heme synthesis enzymesÑeven dysfunctional enzymesÑhave enough residual activity to assist in heme biosynthesis. The principal problem in these deficiencies is the accumulation of porphyrins, the heme precursors, which are toxic to tissue in high concentrations. The chemical properties of these intermediates determine the location of accumulation, whether they induce photosensitivity, and whether the intermediate is excreted (in the urine or feces).'
Secondary Porphyria can also be caused or exacerbated by a Chlamydia pneumoniae infection. Please see the Bacterial Infections page for more information.
Please see the Tests page for more information about measuring Porphyrins.
The effects of impaired Heme production on Oxygen transport and diffusion in the body are also examined on the Insufficient Tissue Oxygenation and CFS page.
The presence of heavy metals in the body is thought to hugely increase the burden of free radicals on the body. Free radicals tend to multiply Ôexponentially' (not mathematically correct) in the body when they strike heavy metal complexes. A free radical hitting a toxic metal ion is thought to multiply by a factor of 1000 or even 1,000,000, producing betweens 1000s and millions of new free radicals. These free radicals will damage proteins in the body unless they are neutralised by the body's natural antioxidants or antioxidant nutrients. One way to avoid excessive free radical damage is to remove toxic metal elements from the body and of course to take enough antioxidants/simulate production of the body's natural antioxidants. Please see the Antioxidants section of the Nutrition page and the links below for more information.
In the process of energy production, magnesium is particularly important in regulating and stabilising ATP, and is often displaced by the presence of heavy metals. Nutritional elements such as Magnesium, Zinc and Selenium have an important role in protecting the body from the effects of heavy metals, and those individuals with elevated heavy metal levels have a greater requirement for these nutrients (and a corresponding great need to detoxify the heavy metals from their bodies). Individuals with heavy metal toxicity tend to have lower levels of these nutritional elements in the body because of displacement by heavy metals. Zinc is important in the formation of metalloproteins and enzymes in the immune system, and Selenium is used in the formation of the natural antioxidant Glutathione. Displacement of these elements can result in deficiencies in these areas.
Above, we have examined the role that Heavy Metals play in combining with protein molecules and preventing the normal functions of those proteins and the bonding of those proteins with intended nutritional metal type which would allow them to function correctly and metabolised for other uses.
Organs affected by Mercury include the nervous system, appetite and pain centres, cell membranes and the kidneys. Systems affected include the transport of sugar (inhibition of), cell membrane permeability of potassium (increase of) etc. Protective nutrients include selenium, vitamin C, pectin and sulphur-bearing amino acids.
The BeatCFSandFMS.org web site contains a reference page with a number of references to source articles regarding the specific effects of mercury toxicity on bodily processes and pathways.
An adverse effect on the immune system's Neutrophils and Leukocytes, reducing the body's ability to fight off bad bacterial, fungal and parasitic overgrowth/infections
An adverse effect on liver enzyme production, involved in both toxin removal and blood creation (i.e. disrupting the Coproporphyrin III Porphyrin isomer, an intermediate to HEME production, a precursor to blood production - please see above)
An adverse effect on brain chemistry:
Blocking the dopamine-beta-hydroxylase (DBH) enzyme, which is used in the synthesis of the noradrenaline (NA) neurotransmitter (NA - a stress hormone is required to maintain energy levels during the day)
Blocking copper catalyzed dithiolane oxidases, e.g. coproporphyrin oxidase (resulting in low copro III seen w/ Porphyrin Analysis) and dopamine-beta-hydroxylase (DBH)
Clogging up the Noradrenaline (NA) alpha-1 receptors, reducing NA communication
Clogging serotonin 5-HT2 receptors
Impair Astrocytic Dopamine uptake
Impair Acetylcholine Esterase function (the enzyme that allows deactivation of cholingeric neurons to return to resting state after activation). Thus, if Acetylchloine Esterase function is inhibited by Mercury, then levels of Acetyl Choline may build up, causing continuous stimulation of the muscles, glands and central nervous system.
Impair cholinergic metabolism (i.e. metabolism relating to the neurotransmitter Acetylcholine)
Studies on mice have revealed that the heavy metal Mercury increase the release of endogenous glutamate (an excitatory neurotransmitter), inhibit glutamate uptake, reduce mitochondrial activity (energy production), and decrease ATP levels.
'Mercury compounds disrupt neuronal glutamate transport in cultured mouse cerebellar granule cells', Elena Fonfria, M.Teresa Vilaro, Zoila Babot, Eduard Rodriguez-Farre, Cristina Sunol (2004).
In the presence of Mercury, Selenium is not able to bind with Glutathione Peroxidase, and so it is not able to assist the antioxidant enzyme Superoxide Dismutase (SOD) in breaking down Superoxide, a free radical produced during energy production. Most CFS patients (if not all) do not produce enough Glutathione on account on methylation problems anyway. The more energy one produces, the more Glutathione one requires. Inadequate levels of Glutathione can result in oxidative damage to the mitochondrial membranes.
According to Doctor's Data Urine Toxic Metals report, based on various sources:
The manifestation of symptoms associated with excessive mercury toxicity can depend on a number of factors:
The chemical form of absorbed Mercury and extent of transport into the body's tissues.
Presence of other synergistic toxins (e.g. Lead, Cadmium)
Presence of a disease that depletes or inactivates lymphocytes (White Blood Cells) or that suppresses the immune system (i.e. immunosuppressive) in other ways
Organ levels of xenobiotic (exogenous toxic) chemicals and (protective) sulphydryl (sulfhydyl)-bearing metabolites, e.g. Glutathione
Sufficient concentration of protective antioxidant nutrients and displacing metals, e.g. Zinc, Selenium, Vitamin E, etc.
Early physiological signs of Mercury toxicity or contamination include:
Impaired senses - touch, vision, hearing and taste
Metallic taste in the mouth
Decreased mitochondrial function - Fatigue decreased endurance
Increased saliva production
A worsening and development of symptoms from moderate or chronic exposure to Mercury may include:
Weight loss or Anorexia
Paraesthesia (a.k.a. Parethesia) - tingling, pricking or numbness of the skin (pins and needles)
Headaches
Hypertension (high blood pressure)
Irritability and excitability
Immune System Suppression and possible Dysregulation
Advanced disease symptoms and processes from Mercury toxicity may include:
Tremors
Loss of coordination
Anemia (decreased number of Red Blood Cells, decreased amount of Hemoglobin in the blood or decreased binding ability of Hemoglobin).
Below is some test report data on a few selected heavy metals. A broader overview of (virtually) all heavy metals can be found in the next section.
According to Trace Minerals International's Toxic Metals Chart, www.tracemin.com:
Arsenic - Excessive levels or a sensitivity to arsenic can affect enzyme function, inhibiting essential enzymes. Damage caused by arsenic can be mitigated to some extent by zinc, vitamins A/C/E, selenium and sulphur-bearing amino acids.
Lead - The chief organs affected are bone, liver, kidneys, pancreas, brain, heart and nervous system. Excessive lead levels or a sensitivity to lead can result in an altered cell membrane permeability, enzyme function, osteoblast production and blood formation. Protective nutrients include calcium, iron, zinc, vitamins C/E and sulphur-bearing amino acids.
Cadmium - Organs affected include the lungs, liver, kidneys, heart and blood vessels, the brain and the appetite and pain centres. High/significant levels can affect breathing, kidney function, block the appetite and smell centre, heart and blood vessel structure (hypertension or hypotension) and calcium metabolism. Protective elements include calcium, copper, selenium, suphur, zinc, vitamin C and amino acids.
According to Doctor's Data, Urine Toxics Metals report, based on various reference sources:
Lead - some of the effects of Lead toxicity include:
Tends to accumulate in the bones, on account of its similarity to Calcium and Strontium in it's +2 electric charge. Here, as mentioned above, it inhibits the formation of Heme and Hemoproteins such as Hemoglobin in Erythroid (RBC) precursor cells in the bone marrow.
Lowever levels of lead accummulation and toxicity can cause a variety of other problems, before Heme production is disrupted significantly, including:
Impaired vitamin D metabolism
Decreased nerve conduction rates
Pediatric developmental problems such as IQ loss, hearing impairment, delayed growth and various behaviour disorders
Synergistic toxicity in combination with other heavy metals, such as Cadmium and Mercury, even at low concentrations of Lead. In pregnant women, transplacental transfer of lead to the foetus can occur at extremely low lead concentrations in the body. Whole blood analyses of lead can only be expected to reflect recent exposures and do not correlate very well with the total body burden of lead. I.V. Vitamin C has also been known to increase lead excretion, besides the obvious choices of chelating agent such as EDTA, DMPA or DMSA.
Bismuth - is only considered to be slightly toxic with ingestion of gram quantities necessary before any visible/detectable signs of toxicity occur. Only 5-10% of soluble bismuth salts are absorbed into the blood when orally ingested. Early signs of Bismuth excess may include constipation or bowel irregularity, bad breath, changes in skin pigmentation, blue-black gum pigmentation with stomatitis (inflammation of mucus linings of mouth). At sub-gram quantities, no toxic effects are (yet) documented for Bismuth. The existence of health problems due to environmental pollution by Bismuth are not documented either. Bismuth has various therapeutic uses with antimicrobial, anti-secretory and anti-inflammatory properties. Bismuth subsalicylate is used in the product Pepto-Bismol, and hydrolyses in the stomach to salicyclic acid and insoluble bismuth. Historically it ws used to treat syphilis. Bismuth has a variety of industrial uses, as well as being found in some lipsticks (e.g. pearlescent white) and paint.
Please see the following chart, provided by Genova Diagnostics, for a list of toxic elements, their sources and their effects. It examines Aluminium, Antimony, Arsenic, Barium, Bismuth, Cadmium, Caesium, Gallium, Gadolinium, Germanium, Lead, Mercury, Nickel, Niobium, Platinum, Rhodium, Tellurium, Thallium and Thorium.
Simply left click, or right click and select 'Save Target'). Viewing this chart requires Adobe Reader. If you do not have this, please download it from the following link.
Please click on the link below for a view of the periodic table, where you can see how the elements all fit together. Chemistry becomes fun when you can apply it directly to yourself!
'Symptoms [of Mercury poisoning] typically include sensory impairment (vision, hearing, speech), disturbed sensation and a lack of coordination. The type and degree of symptoms exhibited depend upon the individual toxin, the dose, and the method and duration of exposure.'
'Arsenic poisoning interferes with cellular longevity by allosteric inhibition of an essential metabolic enzyme pyruvate dehydrogenase (PDH) complex which catalyzes the reaction Pyruvate + CoA-SH + NAD+ PDH Acetyl-Co-A + NADH + CO2 [i.e. energy production or metabolism]. With the enzyme inhibited, the energy system of the cell is disrupted resulting in an apoptosis episode. Arsenic in cells clearly stimulates the production of hydrogen peroxide (H2O2). When the H2O2 reacts with Fenton metals such as iron, it produces a highly reactive hydroxyl radical. Inorganic Arsenic trioxide found in ground water particularly affects Voltage-gated potassium channels , [1] disrupting cellular electrolytic function resulting in neurological disturbances, cardiovascular episodes such as prolonged qt interval, high blood pressure [2] central nervous system dysfunction and death. Arsenic trioxide is a ubiquitous element present in American drinking water.'
'Lead poisoning (also known as plumbism, colica pictonium, saturnism, Devon colic, or painter's colic) is a medical condition caused by increased levels of the heavy metal lead in the body. Lead interferes with a variety of body processes and is toxic to many organs and tissues including the heart, bones, intestines, kidneys, and reproductive and nervous systems. It interferes with the development of the nervous system and is therefore particularly toxic to children, causing potentially permanent learning and behavior disorders. Symptoms include abdominal pain, headache, anemia, irritability, and in severe cases seizures, coma, and death.'
One example of an effect of insufficient Phase 1 oxidative enzymes, i.e. Cytochrome P450 enzymes, is the potential build up of Hydrogen Sulphide in the mitochondria, resulting in inefficient mitochondrial functioning and oxygen respiration, and general fatigue.
An example of exotoxins produced by bad bacteria, parasites and fungi includes Hydrogen Sulphide (Sulfide in the USA), or H2S.
As stated below in the Sources of Exogenous Toxins section, on the Bacterial Overgrowth page and Mitochondrial Dysfunction page, Hydrogen Sulphide (H2S) is an exotoxin produced in the body by the action of bad bacteria and fungi (such as Candida Albicans) fermenting sugar in the gastrointestinal tract. H2S is also natural by product of various bodily processes (e.g. produced by brain, pancreas and GI tract) and it plays a part in regulating the blood pressure, body temperature, vascular smooth muscle,cardiac function, cerebral ischemia, and in modulating the hypothalamus/pituitary/adrenal axis.
Since hydrogen sulfide occurs naturally in the environment and the gut, enzymes exist in the body capable of detoxifying it by oxidation to (harmless) sulfate. Hence low levels of sulfide may be tolerated indefinitely. Humans can smell the odour of hydrogen sulfide at 0.02 ppm. The toxicity of H2S is comparable with that of Hydrogen Cyanide. H2S is characterised by the 'rotten eggs' smell at low gaseous concentrations. Levels of H2S are normally regulated by the body's oxidative enzymes.
Elevated levels of H2S in the blood and tissues, that the body's oxidative enzymes cannot effectively deal with (or being overwise engaged with oxiding drugs and other chemical toxins from the blood in addition to the additional H2S), can result in mitochondrial dysfunction by their action on the Cytochrome C Oxidase enzyme which is involved in ATP production. It forms a complex bond with iron in the mitochondrial cytochrome enzymes, thereby blocking oxygen from binding and stopping cellular respiration.
Recent research has shown that even at low, non-toxic doses, H2S produces a reversible state of hibernation-like deanimation in mice, causing a decrease in core body temperature, an apnea-like sleep state, decreased heart and respiration rates and a severe metabolic drop.
Treatment of severe (toxic and immediately life threatening) cases of Hydrogen Sulphide poisoning (in industrial applications) involves immediate inhalation of amyl nitrite (i.e. 'poppers'!), injections of sodium nitrite (both powerful vasodilators), inhalation of pure oxygen, administration of bronchodilators to overcome eventual bronchospasm, and in some cases hyperbaric oxygen therapy (HBO). HBO therapy has anecdotal support and remains controversial.
With regards to dealing with cases of low (non-toxic) levels of Hydrogen Sulphide poisoning in the body's mitochondria, for example that which arises as exotoxins produced by bad bacteria, fungi and parasites in the digestive tract over long periods of time, then treatment options may include boosting the body's natural oxidative enzyme count and assisting liver functioning; cutting out toxins and drugs that require removal by the Cytochrome P450 enzymes (i.e. alleviating the burden on these enzymes to allw them to focus on removing the H2S movlecules); removing the source of the additional exotoxins (i.e. eliminating the bad bacterial/fungal/parasitic overgrowth that is producing the extra H2S); and proper breathing (i.e. diaphragm breathing rather that the shallow breathing that is typified by use of the rig cage only). Oxygen therapy and even hyperbaric therapy may well be useful too. As mentioned on the Causes and Effects page, I have Technical/Decompression Diving certification and have access to oxygen tanks, and I found that breathing this for short periods of time (on dry land!) considerably helped me feel better and more oxygenated, as if I was breathing before but not getting the oxygen to the tissues and taking part in respiration in sufficient quantities. If one is breathing correctly, with fresh air, regularly, then one cannot really do much more than this, other than raise the oxygen content of the gas one is breathing. Proper breathing is also very important for general health, to expel enough CO2 (raising one's pH and avoiding Acidosis and to raise the blood O2 levels in the haemoglobin in the red blood cells to high enough levels. For low levels of H2S poisoning, it is not recommended to use vasodilators, as one's condition is not life threatening and dilating the blood vessels like this is too severe a solution, the vasodilator chemicals themselves having various adverse effects on the body and being poisons themselves.
Elevated bodily Hydrogen Sulphide levels are said to result in elevated levels of Hydrogen Sulphide in the urine, according to Kenny De Meileir, which forms the basis of a new 2009 home test by Protea Biopharma.
Lipofuscin, a.k.a. lipopigment, is a type of yellow-brown fine pigment granule, comprised of lipid-containing residues of lysosomal digestion. Lysosomes are cellular organelles (separate intracellular substructures) that contain hydrolase enzymes to break up waste materials and cellular debris. It is a form of cellular debris or waste. It can derive from a variety of sources, primarily the glycation of proteins (i.e. a sugar bonding to a protein or lipid molecule without the controlling action of an enzyme) and also as a lipid an protein peroxidation product produced by free radical attack on cellular membranes and protein structures. The results of these rogue reactions are broken down by lysosomes resulting in the Lipofuscin that we are concerned with here.
'An increase in the volume of neuronal lipopigment may indicate increased functional activity of the cell, impaired removal of pigment or anoxia' (i.e. low oxygen levels).
Lipofuscin is not toxic in of itself, but the effect of its presence can have extremely detrimental effects on the cell and accelerate the ageing process. Lipofuscin tends to agglutinate or clump together, forming a sludge - imagine trying to play football whilst wading through water! The agglutination tends to clog up cellular membranes, reduce their fluidity and cause cellular dehydration - resulting in less efficient enzymatic cellular reactions and less efficient DNA and RNA transcription and translation. Lack of cellular membrane fluidity also results in impairment of normal Sodium, Potassium and Calcium transport in and out of the cell, reducing cellular communication (i.e. prevents synapses from releasing neurotransmitters that allow communication of information between nerve cells) and fluid flow. Dehydrated cells tend to dissipate heat less easily from enzymatic reactions. Intracellular temperatures thus tend to increase which also has the effect of increasing the amount of harmful, rogue glycation of proteins, resulting in a vicious circle of Lipofuscin build up and cellular ageing and degeneration. When Liposfuscin levels reach a critical threshold concentration the cell may die.
'[Prof. Imre Zs.Nagy]...discovered that the cells that make up young bodies comprise 92% water and lipids, and 8% dry mass. Conversely, elderly bodies comprise only 40% water and lipids, and 60% dry mass.'
Lipofuscin may also absorb heavy metals such as Mercury and Aluminium as well as nutritional elements such as Zinc and Copper. Lipofuscin is there a matrix in which heavy metals are retained in the cells of the body.
Old mammamls have been demonstrated in some cases to have up to 30% of their cellular mass comprised of Lipofuscin. Lipofuscin build up tends to occur chiefly in the brain, heart muscle, smooth muscle (vascular system, bladder, reproductive tracts, GI tract, lungs, skin and eye).
Glycation products are an intermediary towards the slow formation of Advanced Glycation Endproducts (AGEs). Some AGEs are more reactive than the sugars they are derived from and are implicated in many age-related chronic diseases, e.g. cardiovascular diseases, Alzheimer's Disease, Cancer, Peripheral Neuropathy and sensory losses like Deafness. AGEs tend to interfere with molecular and cellular functioning throughout the body and result in increased oxidants. Long-lived cells such as nerve cells and brain cells, DNA, long-lasting proteins such as eye crystalline and collagen (lining blood vessels), as well as retina cells and insulin-producing beta cells are particularly at risk from damage. 'Browned' foods from baking, frying, grilling, caramelisation, or added AGEs (brown food colouring e.g. caramel in soft drinks like Cola) also are a exogenous source of AGEs.
'As we grow older the cell membrane becomes less lipid (less watery and more solid). This impedes its efficiency to conduct normal function and in particular there is a toxic accumulation. This cellular toxin is referred to as lipofuscin and as we grow older lipofuscin deposits become more present in the brain, heart and lungs and also in the skin. Indeed some of the skin age-pigments referred to as liver or age-spots (brown spots or patches that form on the skin with age) are composed of lipofuscin. It is known that Alzheimer Disease patients have much higher levels of lipofuscin deposits than compared to their healthy controls. The cells declining efficiency also means that the essential and regular transfer of sodium and potassium is impaired, thus reducing communication. It is also believed that electrical and heat transfer is also impaired. Professor Zs-Navy himself became involved in research to find substances that could aid in the removal of lipofuscin deposits and improve cellular lipidity and communication.'
The complete Membrane Hypothesis of Aging bulletin by Prof. Imre. Zs.-Nagy can be read at the link below.
Zs.-Nagy emphasised that when Hydroxyl Radicals (OHRs) - a result of the interaction of Superoxide Radicals (SOR) and Hydrogen Peroxide (H2O2) from respiration - are created in confined, high-density spaces, such as cellular membranes, the probability of intermolecular cross-links increases greatly, rendering the cellular membranes, especially the mitochondrial membranes, most vulnerable to OHR attacks (by a factor of 10). Whilst most cells divide by mitosis as a defense mechanism, certain post-mitotic cells which do not divide are most vulnerable to OHR free radical attacks. These include the brain, heart and muscle cells. Continuous free radical damage to these cellular membranes can result in increased levels of dehydration, as the potassium and water permeability of the membranes decrease, resulting in less water able to get into the cells and less Potassium able to get out.
It is contested as to whether natural mechanisms exist for the removal of Lipofuscin. The idea of lysosomal digestion is to fully break down any waste as much as possible - that is the elimination method. Lipofuscin in the end product of the digestion of certain types of lipid wastes and as such cannot be broken down enzymatically by cells any further.
It is estimated (source unknown) that for Glycation products as a whole, renal (kidney) elimination is only 30% and the half-life of a glycation product is estimated as being twice the life span of the average bodily cell. Lipofuscin levels therefore tend to increase with age, interfering with cellular functioning and communication.
The accumulation of lipofuscin-like material has been induced in rats using a protease enzyme inhibitor, and the elevated levels returned to normal after 3 months. This would indicate a disposal mechanism. However this is not strictly speaking 'true Lipofuscin', and removal of Lipofuscin has not been demonstrated in vitro. There is evidence to suggest that accumulated Lipofuscin cannot be removed from cells in vitro.
The main natural defense against Lipofuscin build up is cell death, when new cells are created (Lipofuscin-free). This may work for short-lived, replicating (mitotic) cells, but not for long-lived cells and proteins, as described above, such as brain and nerve cells etc. This is why Lipofuscin tends to accumulate in the longer-lived cells, proteins and lipid membranes, interfering with their function and causing their premature ageing and degeneration.
As far as I am aware, there are no commercially available tests for Lipofuscin levels. However, one can indirectly measure the effects of Lipofuscin levels in terms of hydration levels (total body water, extracellular water volume and exchangeable Na+ levels by radioisotope methods), plasma volume (PV) measurements (by indocyanine-green dilution test), as well as examining serum lipids and hormone and neurotransmitter levels.
For information regarding Lipofuscin removal, please see the Centrophenoxine section on the Detox page.
There is some evidence to suggest that when the human mind is operating on a higher level that the body has much higher resistance to the damaging effects of toxic, poisonous and carcinogenic compounds, to the point of defying medical understanding. This evidence is based partly on kinesiological testing of a cigarette and virtually all participants were shown to go weak when holding the cigarette whether they smoked or not. Some participants however did not go weak when holding the cigarette and when interviewed were found to have been studying self-development techniques. Kinesiological evidence has to be evaluated carefully as in some instances, the body does not provide a clear answer as it loses clarity. Kinesiological testing is briefly examined on the Identification page.
The same principles apply to fire walking with bare feet. Clearly there are limits to how much the body can take even when the mind is positively influencing it, and a bullet to the head is clearly going to be fatal. But there is a large grey area. Some people clearly exhibit a much greater sensitivity to specific toxins or heavy metals than others in terms of the endocrine system adaptation and immune system response. However, the exact relative influence of qi levels, mental state and beliefs, biochemistry and genetics is not quite clear. They all play a part to some degree. This web site is not recommending that one ignores all the effects of toxicity by having a positive mental attitude and relying on one's belief system. But nor it is recommending that people focus entirely on medical/biochemical treatment and instill solid beliefs into their minds that they are indeed 'dirty' or 'full of toxins' inside their bodies. Instead, it is prudent to attack the problem from all angles, and actually align one's beliefs with the maximum power of the mind, and to achieve higher levels of psychological wellbeing, believing one is already well and clean and free of toxins, but whilst at the same time using all the most appropriate biochemical/herbal tools available (for example, those discussed on this page) to detoxify the body. If one has the mindset that one is already free of toxins, it may clearly 'help' the body to release more toxins rather than to hold them in as the mind has the firm belief that they are there and are hard to shift. This may sound like new age mumbo jumbo, but is doesn't cost anything and why not try it whilst engaging in your detoxification programme?
Some people suffer from sensitivity to specific chemicals or toxins, whilst others suffer from a sensitivity to a broad range of toxins, pollutants or even strong odours (known as 'Multiple Chemical Sensitivity'). Whether this is a result of energetic, genetic, biochemical, immune system sensitivity to certain chemicals or whether it is a result of having been exposed to significant levels of these chemicals over time and built up too many toxins on the cell membranes, in the colon and in the fat cells of the body (and hence an inability to effectively remove any new toxins) is another matter. MCS is examined at the links below.
'Multiple Chemical Sensitivity; in broad terms it means an unusually severe sensitivity or allergy-like reaction to many different kinds of pollutants including solvents, VOC's (Volatile Organic Compounds), perfumes, petrol, diesel, smoke, "chemicals" in general and often encompasses problems with regard to pollen, house dust mites, and pet fur & dander.'
Prof. Martin L. Pall stipulates that MCS is a response to certain organic chemical stressors, as opposed to food allergies that are an immune system response to certain types of proteins that are misinterpreted to be of viral origin. This MCS response to organic chemicals and compounds is caused up excessive NMDA upregulation, a shift in the normal Nitric Oxide/Peroxynitrite cycle, and also impaired liver function (i.e. the capability to process such toxins). Peroxynitrite formation is discussed on the Oxidative Stress page. According to Pall, the main stressors that cause MCS and this shift in the Peroxynitrite cycle in the first place are: Volatile Organic Solvent Exposure, Organophosphorus/carbamate Pesticide exposure, organochlorine pesticide exposure, pyrethroid exposure, hydrogen sulfide exposure, carbon monoxide exposure and mercury exposure. Toxicity build up from these sources in combination with an oveburdened liver can thus produce the symptoms of MCS.
Martin Pall has suggested that exposure to the following toxic compounds (cumulative effect over long term, low level exposure (or one or more) or a single high-level exposure incident - or consecutive incidents) are implicated in the initiation of the illnesses of CFS, ME, Multiple Chemical Sensitivies, Fibromyalgia by stimulating the Nitric Oxide/Peroxynitrite cycle:
Organophosphorus Pesticides - CFS, ME, MCS - one of most common causative factors
Carmbamate Pesticides - MCS
Organochlorine Pesticides - MCS
Pyrethroid Insecticides (Commercial and Domestic) - MCS
Volatile Organic Solvent Exposure - MCS - one of most common causative factors
Mercury - MCS
Ciguatoxin (a type of poison found in reef fishes whose flesh is exposed to toxins produced by dinoflagellates (a type of plankton)) - CFS, ME
Of course, individual cases may well have more than one stressor and not necessarily as classified above. These comorbid conditions are fluid and vary in their progression and exact nature according to the individual.
Whilst heavy metal toxicity, inefficient liver function and elevated peroxynitrite levels may well be responsible for the majority of MCS symptoms, it is likely that the immune system is also implicated, in a form of secondary immune system response, often related to the GI tract. This is discussed on the Food Intolerance page.
A healthy functioning immune system should have a healthy balance between Th1 (white blood cells) and Th2 (antibodies) activity. An immune system out of balance, e.g. Th2 overactivation, may well produce the symptoms associated with MCS and indeed certain auto-immune diseases. In some respects MCS can be considered to be the immune system over-reacting to foreign toxins, allergens, normal bacteria and parasites, and under-responding to viri, harmful yeasts, harmful intracellular bacteria and even cancer.
Dr Mark Donohoe stipulates that multiple chemical sensitivities are often instances of toxic damage or excessive neurotoxins present in the lipid compartments of the body, in particular the brain. This results in disruptions to endocrine function and immune function. These may be present perhaps because of reduced liver function (caused by over burdening and/or a build up of toxins or parasites in the liver interfering with its normal functions).
The book 'Killing Us Softly: Chemical injury & chemical sensitivity' by Dr Mark Donohoe can be downloaded at the link below (on his web site).
The skin is one detoxification medium of the body. In a human's natural state, the skin and muscles are soft, elastic and rubbery. In an average adult they are stiffer and more rigid, without as much elasticity, and there is much more subcutaneous fluid. Only by cellular detoxification can one restore the skin and tissues natural state. It is clearly much cheaper and more effective to perform a full bodily detoxification than it is to spend money on regular skin treatments in order to restore one's natural soft skin feel and rich complexion. One other factor in skin softness and elasticity is one's internal energetic system. With a good flow of qi throughout the body, the skin will become much softer. Cellular toxification is probably one of the biggest causes of ageing and cancer. If you want to look young and feel great in your old age, then you need to detoxify your body! It isn't enough just to exfoliate the skin using expensive skin products and treatments, whilst leaving the rest of your body full of toxins.
By all means spend your money on skin treatments if you find it enjoyable and relaxing, but remember that it should not be a substitute for a proper cellular detoxification programme.
Is your body a Temple? Or is it the Temple of Doom??
Some techniques for drawing toxins from the skin and exfoliating the skin can be found in the Skin Cleansing section below. Skin Cleansing is of course only one part of an overall detoxification programme.
Free radicals damage the mitochondria (that produce the body's energy). Free radical damage shorts the life of our bodies cells and contributes to premature ageing. The number of times our somatic cells can replicate or divide are fixed or rather limited. The protective telomeres present at the end of chromosomes become shorter each time a cell divides. The telomeres maintain the viability of body/somatic cells. When they are too short they can no longer protect the chromosomes or provide the cell with the ability to divide. When the telomeres of the chromosomes that make up a cell are lost, the cell undergoes apoptosis or perish. Thus, increasing the length of the life of each cell prior to division (by consuming enough antioxidants and minimising the number of oxidants consumed/breathed in/built up in the body (i.e. toxins)) contributes to increasing one's overall life expectancy and delays the onset of ageing.