Feeding Programs for Laying Hens: Fatty Liver Syndrome
The condition of fatty liver in poultry has been observed for quite some time. While it is true that an alteration in liver function can lead to a build-up of fat in the liver, many cases of fatty liver in laying hens can be traced to an imbalance in nutrient intake. Low protein, high energy diets and those in which there is an amino acid imbalance or deficiency can be major contributors to a fatty liver condition in layers. It is known that diets low in lipotrophic factors such as choline, methionine and vitamin B12 can result in fatty infiltration of the liver.
However, these nutrients are seldom directly involved in most of the fatty liver problems reported from the field. Excessive feed intake (more specifically energy intake) is also a major cause of the condition. It is well known that laying hens will overconsume energy, especially with high energy diets and this is particularly true of high producing hens. Pullets reared on a feeding program that tends to develop a large appetite or encourages "over-eating" (high fiber diets or skip-a-day feeding), are often more susceptible to the condition when offered a high energy diet on a free choice basis during lay. There is some information to suggest that daily fluctuations in temperature, perhaps affected by the season of the year, will stimulate hens to over-consume feed. Hence, it is important to attempt some type of feed restriction program if feed intake appears to be excessive.
When fatty liver is a problem, adding a mixture of so-called "lipotrophic factors" to the diet is often recommended. A typical addition may involve 60 mg CuSO4, 500 mg choline, 3 μg vitamin B12 and 500 mg methionine per kg of diet. It should be emphasized that in many cases, the addition of these nutrients will not cure the problem. Increasing the level of dietary protein by 1 to 2% seems to be one of the most effective ways of alleviating the condition. However, such treatments do not work in all cases. Another treatment that may prove effective is to increase the supplemental fat content of the diet. This apparently contradictory move is designed to offer the birds a greater proportion of energy as fat rather than carbohydrate. The idea behind this diet manipulation is that by reducing carbohydrate load there is less stress on the liver to synthesize new fat required for egg yolk production. By supplying more fat in the diet, the liver merely has to rearrange the fatty acid profile within fats, rather than synthesize new fat directly. For this treatment to be effective, the energy level of the diet should not be changed, the recommendation merely being substitution of carbohydrate with fat. This concept may be the reasoning for apparent effectiveness of some other treatments for fatty liver syndrome. For example, substitution of barley or wheat for corn has been suggested, and this usually entails greater use of supplemental fat with these lower energy ingredients. Similarly, substitution of soybean meal with canola or sunflower meals usually means using more supplemental fat if energy level of the diet is to be maintained.
More recent evidence suggests that mortality is caused by eventual hemorrhaging of the liver, and that this is accentuated or caused by oxidative rancidity of the accumulated fat. On this basis, we have seen a response to adding various antioxidants, such as ethoxyquin and vitamin E. Adding ethoxyquin at 150 mg/kg diet and extra vitamin E up to 50-60 IU/kg has been shown to reduce the incidence of hemorrhage mortality.
Experience has shown that it is difficult to increase production in a flock once the condition is established. Thus it is important that a proper program be followed to prevent the development of fatty livers. In some cases, the cause of the trouble can be traced back to pullets coming into the laying house carrying an excess of body fat. If these birds are then subjected to a laying diet in which the balance of protein and energy is slightly suboptimal for a particular strain of bird, a build-up of fat in the liver may occur. Also, the feeding of crumbles or pellets in the laying house may aggravate this condition, since the hen may overeat such rations if offered on a free choice basis.
Recent information suggests that a condition similar to the so-called fatty liver syndrome may be caused by certain types of molds or mold toxins. Although no definite relationship has been established to date between molds and fatty livers, care should be taken to ensure that molds are not a factor contributing to poor flock performance. From time to time, canola meal has been implicated with the fatty liver syndrome. While it is true that there were earlier reports with some of the high glucosinolate rapeseed meals triggering such a condition, there is no evidence to suggest that the new canola varieties are a factor in the fatty liver condition. Hemorrhage due to rapeseed is usually not associated with excess fat infiltration of the liver.