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      injected heroin.  When the heroin is removed, that weight is
      unbalanced and it begins to produce the constellation of symptoms that
      are known as withdrawal symptoms, or "drug sickness."

      The symptoms begin with vague uneasiness and irritability.  But as the
      time from the last dose increases, they include sweating and chills,
      nausea and stomach cramps, which progress to nausea, vomiting and
      diarrhea; diffuse muscle and joint aches and pains.  None of these is
      catastrophic by itself, but when the complete syndrome is established
      and getting progressively worse, it drives the person to seek relief in
      the form of another injection or  dose of heroin which will quickly
      restore the balance and relieve the symptoms, making them feel more
      normal.  As the months and years of addiction slide by in the twilight
      mental state of addiction, the person obtains less and less of the
      positive incentive of the high and more and more of the negative
      misery of withdrawal.  And so ultimately, it is the brain's defense
      against the continuous onslaught that becomes the engine that drives
      the dynamics of addiction.

      Methadone is effective because, after a single oral dose, it occupies the
      opiate receptors and prevents withdrawal symptoms.  Further more,
      when an adequate dose is established, it prevents the craving for
      heroin that fuels the continuing compulsion to seek the drug.

       Why Do We Have Opiate Receptors?

      This question came up earlier, and it is a very important question.  If
      evolution has selected for those characteristics that make it possible to
      survive on this planet, why would  our genetic code provide for the
      synthesis of a structure that responds to interaction with a substance
      found in one particular plant?

      In the early 1970s scientists discovered that there were specific sites in
      the brain of mammals that would bind morphine and other opiates that
      were labeled with radioactive markers, and that these sites were
      located in specific areas of the  brain that were involved in the
      perception of pain.  They began to postulate that these receptors were
      actually intended to be interacting with a substance produced by the
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