Some more info and thoughts on fatty liver disease (FLD):
Ben Bikman is an excellent source of info on metabolism. He's a researcher and educator whose work "explores how calories and hormones shape body weight, chronic disease, and overall well-being."
I've listened to several of his podcasts regarding human metabolism, insulin resistance and fatty liver. Here is an excellent overview of fatty liver disease:
Note an important comment from that video:
Insulin resistance is required to create fatty liver disease.
"Insulin resistance, a key player in metabolic disorders, is dissected into two components: impaired insulin action and chronically elevated insulin levels (hyperinsulinemia). Dr. Bikman highlights the crucial role of insulin in driving fat accumulation in the liver, explaining that elevated insulin is necessary for the liver to store fat and prevent its breakdown, even in the presence of excess free fatty acids. He elucidates how insulin resistance in fat cells leads to increased release of fatty acids, exacerbating fat accumulation in the liver."
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That's in people, of course. So then I found this great article -
Avian Liver: The Forgotten Organ
If you're familiar enough with human metabolism and physiology, it's straightforward(-ish) to understand what is being said about avian liver. There are a lot of gold nuggets throughout the various intro sections, including how quickly the liver utilizes fat in response to fasting, how different feed compositions impact fat deposition, and how nutrient density impacts liver weight.
The especially relevant tidbit is under the heading, "Fatty Liver Haemorrhagic Syndrome (FLHS)", which is a type of fatty liver disease specific to chickens. Like other forms of fatty liver, the condition is primary characterized by excessive fat accumulation in the liver. There are a few different hypothesizes as to exactly why FLHS occurs, but I've copy/pasted an excerpt from the article below my comments (bolding/underline are mine).
Okay, so parrots are not chickens, but we have to work with the research that has been done. What we can see here is that the biology of the avian hepatic system has considerable overlap with human biology - and we know a lot about human biology.
In the context of fatty liver disease in people, we know that prolonged elevated insulin (i.e. insulin resistance) is
required to produce fatty liver disease. (The mechanism is clearly explained in the Bikman video.)
Why do we have insulin? How can we lower it?
Insulin plays an important role in regulating blood sugar levels and dictates how energy is utilized. When we eat - particularly, when we eat carbohydrates - our blood sugar rises and the release of insulin is triggered to facilitate glucose uptake by cells for energy. Put simply, when insulin is high, circulating fatty acids (ie. energy) are driven into storage (as fat). When insulin is very low, the body releases those fatty acids for use as fuel.
Lots of things can trigger an insulin release, but large insulin spikes (and bouts of fat storage) are driven by carb consumption. Whole foods with fiber or fat have a smaller insulin response. Exercise after eating can further lower the insulin response. Having more muscle mass, in general, is also better for glucose control as skeletal muscle processes a lot of glucose and can increase glucose sensitivity (
source).
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In thinking about what to do for my birds, I've thought a lot about how metabolism works in people and what would make sense for birds. I've also thought about the references made to historical high instances of fatty liver disease. I can't find the actual data to explain what a 'high seed diet' is, so I can't do much with that information. However, a 'seed diet' is frequently a mix of seeds and grains.
Part of my conure's diet is a 'healthy' seed mix. It contains carbs - canary grass seed, millet, oat groats, veggies and fruit. It also has fattier seeds and nuts, as well as some flaxseed and peas to boost protein.
Looking at Zupreem natural, a popular pellet choice (also, I fed the fruity version to my grey for years and years), we have a very similar breakdown - ground corn, millet, oat groats, barley and wheat for carbs. Vegetable oil and ground flaxseeds for fat. Added fiber. Soybean meal for extra protein.
With the exception of the source of fat, they are very similar.
It probably bears repeating: Eating fat doesn't cause fatty liver.
Insulin resistance leads to fatty liver disease. Both pellets and seed mixes have carbs, so both will lead to increased insulin levels. The carbs become problematic when there is never the opportunity for the insulin level to come down (i.e. periods of no carb availability) or when exercise is so low that there is little demand on the body to release those stored fats as fuel.
I think the real culprit here is high carb in the absence of exercise. Most young people and active animals can eat basically anything and their bodies will burn through it. If you remove exercise from the equation while continuing to feed readily stored nutrients (carbs), you're going to get an animal that becomes overweight and can develop fatty liver.
Info from the avian article:
"Fatty liver syndrome occurs when high producing hens are in over-supply of energy or a positive energy balance, but the presence of these conditions does not guarantee the appearance of FLHS [
96,
146]. Butler [
151] suggested that excess fat in the liver
arises mainly from increased lipogenesis rather than from dietary lipids. Although there has been no constant association with a particular type of diet,
some studies have indicated that high energy diets, especially maize or wheat diets produce higher incidences of FLHS [
146,
152,
153,
154].
Jensen et al. [
155] also stated that the amount of fat deposited in the liver is influenced by the cereal used as the basis of the diet. For instance, with iso-caloric diets based on maize, wheat or barley, the incidence of subclinical FLHS and liver lipid concentration was observed to decrease in that order [
153].
Similarly, the inclusion of such ingredients as fermentation residues, wheat bran or alfalfa have been found to significantly depress liver lipid concentrations [
156]. Olomu et al. [
157] reported that the incidence of liver FLHS tends to increase with the amount of rapeseed meal in the diet due to the erucic acid or other toxic metabolites which can affect the strength of the connective tissue in the liver [
158,
159].
Earlier finding by Hemsley [
160] and Payne et al. [
161] showed that the syndrome was due to biotin deficiency. Frigg [
162] reported that very little of the biotin present in wheat, and some other cereals, is available to the chicken. Therefore, diets based on large proportions of these feedstuffs contain sub-optimal concentrations of available biotin and hence require to be supplemented.
There is evidence that among the mycotoxins, aflatoxin can cause fatty livers in laying hens [
163]. Other fungal metabolites are known to possess
oestrogenic activity and it is possible that their presence may cause the occurrence of the FLHS. Dietary modification can be used to prevent or treat FLHS.
Substituting carbohydrate with supplemental fat might be beneficial.
Hepatic steatosis prevalence in caged birds is believed to be associated with the
lack of exercise combined with a high feed intake in this housing system [
164,
165,
166,
167]. Shini et al. [
167] demonstrated that hens in cages had significantly higher body weights than barn and free-range systems birds. This presumably causes a positive energy balance induced from a lack of exercise due to restricted space in cages.
