Ketosis : Ketosis: What is it Actually, and How Does it Happen?~ Sue Reith

Discussion in 'Health & Wellness' started by Sondra, Oct 25, 2007.

  1. Sondra

    Sondra New Member

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    Thank you Sue for allowing us to post your articles.

    KETOSIS: What is it Actually, and How Does it Happen?
    (Revised 6/03)
    By Sue Reith.

    (Please feel free to give a copy of this article to your veterinarian if
    you would like to do so.)

    Ketosis is a word that (indiscriminately in my view) gets bandied about a
    lot, and it's incorrectly said to be the primary cause of a number of
    ailments. One that comes to mind, because I see it mentioned a lot, is
    "Pregnancy Ketosis". There's no such thing! There's pregnancy, which is one
    condition, and there's ketosis, which is an entirely separate condition.
    Ketosis can develop as a secondary condition under some circumstances
    during pregnancy or lactation, but it isn't limited to either pregnancy or
    lactation, and it can show up at any stage in the life of a goat. (BTW:
    ketosis happens to people, too.)

    The word itself is not well understood, so I'll try to explain it: In
    technical terms, it's a condition brought on by a metabolic imbalance. In
    scientific terms it's defined as an accumulation of excessive amounts of
    ketone bodies in body tissues and fluids. 'Ketone bodies' are metabolic
    substances known as acetoacetic acid and beta-hydroxybutyric acid. Acetone,
    which puts off the peculiar odor associated with Ketosis, comes from
    acetoacetic acid. These substances are all normal metabolic products of
    'lipid' within the liver. When they become severely imbalanced as the
    result of ketosis, the liver will fail.

    Cause: By its very nature, Ketosis has to be a secondary condition, because
    it's the direct result of a process that starts when the animal, for
    whatever reason, stops eating. Why the animal stopped eating is the
    primary question that needs to be answered so the cause can be corrected.
    And that cause must be dealt with quickly, because when the animal stops
    eating, the lack of an outside energy source forces it to start living on
    its own reserves to provide the necessary energy.

    These reserves are in the form of fatty tissue. In the words of Dr WC
    Allenstein, DVM, a cow vet that wrote for Hoard's Dairyman for many years,
    "When this fat utilization occurs, free fatty acids are released into the
    blood stream and are used by the liver for energy. If this occurs at too
    fast a rate, the liver is bombarded with too many fatty acids, and there is
    an increase in ketone bodies released into the system. At a certain level
    the classic symptom of acetone odor on the breath and in milk [if the
    animal is lactating] will occur... The ketone bodies formed by incomplete
    fat metabolism by the liver create these symptoms." He goes on to say:
    "Today we know that anything that disturbs the body - other diseases,
    missed feedings, conditions disturbing feed intake, will create ketosis."

    Lori Ward, then a student in Dairy Sciences at the University of Wisconsin,
    noted in an article that when the animal is forced, by lack of an external
    energy source, to turn to its own body for sustenance, "The body fat is
    mobilized to supply needed energy. The mobilized fat is processed in the
    liver, and it tends to accumulate. In most fatal cases the post mortem
    findings reveal a fatty liver. During fat mobilization, ketone bodies (one
    of which produces acetone) are produced and circulated in the blood, hence
    the names 'ketosis' or 'acetonemia'." Lori notes that most of the accepted
    ketosis treatments attempt to raise blood glucose in some manner. This
    provides a quick energy source for the victim, ending its need to live on
    its own fat reserves to survive.

    A classic example of how ketosis gets involved (and often is the only
    disorder that gets recognized and treated, the end result being the loss of
    the victim's life) is found in an article I wrote on Hypocalcemia. When a
    pregnant doe is being fed a dangerously imbalanced ration and stops eating
    a large part of that ration to instinctively try to correct the imbalance,
    the loss of this external energy source causes her to her turn to her own
    body's resources for survival. Since the babies are still growing in her it
    is very important to fix the original nutritional imbalance, which in this
    case is a diet-induced calcium deficiency. The fetuses inside of her are
    draining her of her own calcium, because of which she loses her muscle
    tone. Without calcium she becomes very weak. So she has weakened muscles,
    including the heart muscle, and at the same time is living on her own body
    reserves because she has stopped eating (and soon is too weak to eat) her
    imbalanced ration. When a pregnant doe becomes hypocalcemic and is
    misdiagnosed by a veterinarian who doesn't understand the dynamics
    involved, he fails to give her calcium replacement therapy at the same time
    that he is reversing the ketosis with energy replacement substances such as
    propylene glycol or Nutridrench. The result is a drained and weakened
    system despite the treatment for ketosis, and she inevitably dies either of
    'unexplained' causes, or of what the vet labels 'milk fever', or 'pregnancy
    toxemia', or 'pregnancy ketosis', or 'parturient paresis', all of which are
    misnomers. Then if he does a necropsy he will generally label the cause of
    death 'liver failure'. I don't agree that liver failure is the actual
    'cause' of death. I see it as the 'result' of the animal's not having been
    diagnosed and treated for both the primary cause, hypocalcemia, and the
    secondary cause, ketosis, because of which she dies. The liver failure,
    then, is not the cause of death, but simply the end result. Ketosis is the
    secondary condition involved. The survival of the animal is dependent upon
    the discovery and correction of the primary condition.


    (While I urge you to share this information with other individual goat
    owners, please do not reproduce the article for publication without my
    specific permission. Thank you. Sue Reith.)

    Sue Reith
    Carmelita Toggs
    Bainbridge Island WA