Forms of Mercury Toxicity

Forms of mercury toxicity

Acute toxicity

  • Environmental, industrial accidents, or terrorist acts (9/11)
  • Accidents – broken Hg thermometers or Hg lamps
  • Iatrogenic (caused by medical treatment itself): vaccinations with ethyl mercury (controversial) and other medications

Chronic toxicity

  • Amalgam fillings
  • Professional hazards — work in dental office
  • Passing from mother — through placenta and through breast feeding
  • Consuming contaminated food (large predatory fish)
  • Polluted environment
  • Multiple vaccinations (controversial)

How Mercury Causes Brain Neuron Degeneration

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5 minute video, copyright University of Calgary 2001

Signs of mercury toxicity

Gross

Ataxia, intention tremors, uncoordinated, dysarrthria (inarticulate speech), psychomotor retardation

Subtle

  • Motor affects: progressing incoordination, imbalance and fine motor tremors in muscles that perform fine motor control like fine tremors of the tongue, lips or outstretched fingers.
  • Hypersalivation (excessive saliva) with pooling of saliva
  • Cold but erythematosus (reddish) hands and feet
  • Unstable, changeable mood (emotional lability)
  • Insidious loss of mental capacity (progressively affecting memory and logical reasoning)

A personality characterized by irritability, anxiety, depression, and restlessness, with lapses in concentration, memory and cognitive function

When to suspect mercury toxicity

  • Clinical picture which is characterized by: neurological, psychiatric symptoms or unexplained symptoms, like fibromyalgia, chronic fatigue, treatment resistant depression, anxiety or Obsessive Compulsive Disorder
  • Mercury fillings in childhood and adolescence, or more than 3 fillings in adulthood
  • Metal taste
  • Tremor
  • Erethism

How come some people have toxicity issues and others do not?

We all are different. There are several factors involved that can affect how and if we manifest symptoms of toxicity:

  1. How exposed we are to toxic metals:
    1. how many fillings we have in our mouth;
    2. how big they are, or how early in life they were put in;
    3. how much large predatory fish we are consuming;
    4. are there other metals in our mouth, such as gold or metal crowns;
    5. are we consuming any other heavy metals in foods or from our surrounding environment?
  2. Is our body overloaded with different toxins that prevent us from being able to excrete them appropriately?
  3. Does our diet support healthy defenses and elimination?
  4. Are we under excessive stress psychologically, spiritually and/or physically?
  5. Was our health affected by excessive vaccinations negatively affecting our immune system?
  6. Were we physically or sexually abused in our childhood?

All of the above factors can have a tremendous effect. The last factor would be our genes.

Apoliprotein E significance

Apoliprotein E (APO E) has been strongly implicated as a risk for developing Alzheimer’s disease. There is also a connection to heavy metal toxicity.

Apoliprotein E (APO E) has 299 amino acids with different ratios of cysteine and arginine at positions 112 and 158.

APO-E2 has 2 cysteins, APO-E3 has one cysteine and one arginine and APO E4 has two arginines. Arginine, unlike cysteine looks at the sulphydryl (SH) groups to potentially bind bivalent metals such as mercury, lead, copper or zinc. It becomes a logical possibility that metal accumulation increases in those chronically exposed individuals who had not inherited APO- E 2.

Lack of sulphydryl (SH) groups to bind bivalent metals such as mercury, lead, copper or zinc increases the accumulation of heavy metals. (Roses, AD, et “Apolipoprotein E genotyping as a diagnostic adjunct for Alzheimer’s disease”. Int Psychogeriatrics. 119; 9 (suppl 1)277-288 and 317-321)

Distribution of Apoliprotein genotype in the population was examined in New Zealand by M. Godfrey:

1-2% of the population has homozygous APO-E4/4. 20% has heterozygous APO—E3/4, 50-60% has APO-E3/4; Reminder: E-2/2, E- 2/4, E-2/3. Chronic mercury toxicity is more common among people with APO-E 4/4 and APO- 3/ 4. (M. Godfrey, et. “Apolipoprotin E genotyping as a potential biomarker for mercury neurotoxicity”. J. of Alzheimer’s Diseases 5 (2003)189-195)

How to diagnose mercury toxicity

  • Acute toxicity (poisoning) by blood, urine and stool testing – only valid for 30 to 60 days following acute toxicity. This form of toxicity is very rare in everyday life. If we test routine blood, stool or urine from the patient, there will be no elevation in the mercury level; therefore, doctors may assume that there is no mercury toxicity. This test will be negative in cases of chronic toxicity. However, this is the test most frequently used by conventional MD’s. This may explain why most cases of chronic toxicity are missed.
  • To diagnose chronic toxicity we should use:
    • Urine random / provocation testing
    • Hair testing (controversial and most of the time negative; it is illegal in NY)
    • Stool random / provocation (difficult to collect)
    • Urine porphirin testing — not well established
    • Kinesiological testing — it is the least proven test; its accuracy depends on the tester. (It is my favorite test to see if toxicity is present and is later used to track the progress of chelation.)