Khia
New Member
- Messages
- 13
Yes, they did some samplings in natural habitats, but this is missing the point.
When an organism is basking in full sunlight (ie. not in shade, nothing between the animal and the sun but atmosphere) then the intensity of UV they experience is by no means a function of the plant structure and water cycle of their environment (ie. what basically creates the microclimate they are in). The intensity here is a function of the latitude, altitude, and general air "quality" (ie. how much atmosphere the UV has to pass through before reaching the animal). To say that it is a matter of whether the animal lives in a desert or a rainforest is patently absurd: the plants on the planet do not dictate to the sun how much UV it produces on that little patch of Earth.
Now, when NOT basking in full sunlight, this is where Fergusson zones come into play, indicating the general UV the animal receives from scattering in the atmosphere, reflectance off of other surfaces, the amount of time spent in those areas, etc. This is what I typically call ambient lighting (vs. the basking lighting).
Most hobbyists take the Fergusson zones as the "sole" UV exposure they should be aiming at. As long as they are in the "zone", they are "good". This neglects what Fergusson has actually stated , and what research has demonstrated, that there should be different zones set up. If you have a basking type reptile, you should be aiming to set up a high intensity basking zone that the whole animal can sit in. The Fergusson zones are a goal to reach for outside that area. This is due to the fact that we've come to understand there are basically 2 roles to what UV does for vitamin D3. The first is the one most hobbyists are aware of: it dramatically increases the rate of conversion of basic vitamin D3 to a form that is what is used in the body (many like to say it creates vitamin D3 and this is inaccurate - it takes what is already there and modifies it at a faster rate to a form the organism actually uses, this can still take place without UV, but does so at a much drastically slower rate, a rate that is possibly not sufficient to support the physiology of the animal). This form is lipid soluble and active, which means it can be stored up in lipid-rich tissues and continues to interact with the physiology of the animal. Which further means it CAN reach unsafe, even deadly levels. This is what is called hypervitaminosis D3.
The second role of UV with regard to vitamin D3 is when sufficient levels of vitamin D3 is attained and if there's sufficient intensity of UVB, it FURTHER converts that modified vitamin D3 into two other compounds, lumisterol and tachysterol. These are basically inert, although the one is thought to have function in preventing tumor growth. In other words, these can be stored safely without reaching hypervitaminosis and actually serve a function in preventing pathologies. They can be converted back to usable vitamin D3 as needed. This is really the only method we know of that animals have for regulating vitamin D3 levels. The effectiveness of this second function is a factor of the compound density in the animal as well as the intensity of the UVB.