Ketosis: What It Is and How It Happens
By Sue Reith
Ketosis is a word that gets bandied about a lot, indiscriminately in my view, and it is incorrectly cited to be the primary cause of a number of ailments. One that comes to mind, because I have seen the term mentioned a few times lately, is "Pregnancy Ketosis". There is no such animal! There is pregnancy, which is one condition, and there is ketosis, which is an entirely separate condition. While under some circumstances during pregnancy or lactation a ketosis can develop as a 'secondary condition', it is neither limited to pregnancy nor to lactation, and can show up at any stage in the life of a goat. (Ketosis happens to people, too.)
It occurs to me that the actual meaning of Ketosis is perhaps not well understood, so I will try to explain it:
A technical explanation of the process would be: Ketosis is a condition brought on by a metabolic imbalance. In scientific terms it is defined as an accumulation of excessive amounts of ketone bodies in body tissues and fluids. 'Ketone bodies' are the metabolic substances acetoacetic acid and beta-hydroxybutyric acid. Acetone, which puts off a particular odor associated with Ketosis, arises from acetoacetic acid, becoming a symptom when the animal is in a ketotic state. All of these substances are normal metabolic products of 'lipid' within the liver. When they become severely imbalanced as the result of ketosis, an end result is liver failure.
Ketosis, just because of what it is, is a secondary condition. The process that leads to it begins when the animal, for whatever reason, stops eating. This action is the primary factor that must be addressed. Without this initial act, ketosis would not happen at all. And it must be dealt with quickly, because when the animal stops eating, the sudden lack of an external energy source causes it to turn for survival to its own body's reserves for a replacement source of energy. These reserves are in the form of fatty tissue. In the words of Dr. W.C. 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. ... Today we know that anything that disturbs the body - other diseases, missed feedings, conditions disturbing feed intake, will create ketosis."
In another article, written by Lori Ward, then a student in Dairy Sciences at the U of Wisconsin, she notes 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. The purpose of this is to provide a quick energy source for the victim, ending its need to live on its own body fat reserves as a means to survive.
A classic example of how ketosis gets involved (and apparently gets all the credit!) is found in my article, 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 makes her turn to her own body's resources for survival. Since the babies are still growing in her it is extremely critical to fix the original nutritional imbalance, which in this case is a diet-induced calcium deficiency. Aside from having fetuses inside of her that are draining her of this calcium, it also has a deleterious effect on 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 in this fashion and is mis-diagnosed by a vet who doesn't understand the dynamics involved, and as a result she fails to receive calcium replacement therapy COMBINED with energy replacement substances such as propylene glycol or Nutridrench, with the result being a drained and weakened system AND ketosis, 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. And if he does a necropsy he will generally determine that the cause of death was 'liver failure'. I cannot agree that liver failure should be considered the actual 'cause' of death, but rather the 'result' of the animal's not having received a proper diagnosis and treatment for the actual combination of the primary cause, hypocalcemia, and the secondary cause, ketosis, because of which she dies. Liver failure, then, is not the cause of death, but simply the end result. The Ketosis is the secondary condition involved. Discovery of the primary cause is always of paramount importance to the survival of the animal.
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|Sue Reith, a retired educator, began raising dairy goats 30 years ago under the Carmelita Toggs herd name. She has written numerous articles on nearly all aspects of caprine management for a variety of goat journals and the Internet. I am pleased to be able to offer some of her material here.
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