I think it is quite clear how I view insulin detemir. Kindke was unable to resist finding the link to the abstract with the diametrically opposing view. I'll just stick both links in here to keep them together, so people can look at both research findings and draw their own conclusions.
Insulin detemir is not transported across the blood-brain barrier.
Insulin detemir is transported from blood to cerebrospinal fluid and has prolonged central anorectic action relative to NPH insulin.
I think it is reasonable to assume that at least one of these two papers is factually incorrect.
If you search on Begg and Woods as co-authors you will find papers redolent with words like "reward", "hedonic" and "dopamine". That's Begg and Woods, if anyone can stomach it.
I was, in my normal confirmation biased way, much more interested in the sort of work produced by Banks, Morley and/or Mooradian. These folks appear to be scientists rather than psychiatrists and they have some great publications. They include major work on the blood brain barrier, leptin transport, insulin transport, leptin resistance, gerontology, diabetes, antioxidants, the list goes on and on.
Here are a few little gems I particularly enjoyed in abstract form which might be worth a mention.
I dislike antioxidants. This is quite interesting from Banks and Morley:
Effect of alpha-lipoic acid on memory, oxidation, and lifespan in SAMP8 mice.
Alpha lipoic acid is a mitochondrial component present in normal cells and is available in mega doses as a supplement. It's a serious and deeply mitochondrial penetrative antioxidant. It helps a lot with diabetic neuropathic pain. SAMP8 mice are oddities which have been bred for early onset senility and memory loss. They are used (probably totally inappropriately) for Alzheimers Disease research. Treating them with antioxidants improves their memory performance. You might think this is a good idea. The cost is measured by a shortening of their life as elderly SAMP8 mice from 34 weeks to 20 weeks after start of treatment (started at 11 months of age). This may or may not be a good thing if you are an SAMP8 mouse (death might be a release). How it applies to a person managing their diabetic neuropathy or trying to delay the progression of their Alzheimers Disease is fascinating and slightly worrisome. I'll stick to a life based around beta oxidation, normglycaemia and a little superoxide signalling, stuff the antioxidants. Last sentence of the abstract "These findings are similar to studies using other types of antioxidants". Sweet, provided you avoid sugar. And antioxidants.
The next snippet includes Morley and Mooradian as authors and relates to making your blood sweet, literally this time, using intravenous glucose:
Mechanism of pain in diabetic peripheral neuropathy. Effect of glucose on pain perception in humans.
Simple hyperglycaemia in a normal person reduces the threshold for feeling pain. It reduces the severity of pain you can tolerate. This applies to a normal human being on a glucose infusion or a diabetic person on a diet designed by a diabetologist, no glucose infusion needed. If hyperglycaemia makes a tolerable stimulus in to a painful experience and makes just bearable pain become unbearable, how many chronic pain syndromes would go in to remission with sustained normoglycaemia? Fat phobia makes this question currently un-answerable. The paper was published in 1984. Does anyone fancy having a gangrenous foot amputated for diabetic complications and waking up on a dextrose saline infusion in recovery? And then being offered the "diabetes diet" on the post op ward?
Banks and Morley were also instrumental in the generation of data for the concept that trigycerides in plasma induce leptin resistance at the blood brain barrier, a few years old now but still quite a useful concept:
Triglycerides induce leptin resistance at the blood-brain barrier.
I find the cream bashing in this last paper a little distasteful and I have to admit that Banks appears to be unaware that high saturated fat low carbohydrate diets are THE way to reduce fasting trigycerides in real people. Can't have everything I suppose. But even if the cream effect applies to people, who cares if I am leptin resistant with a full stomach provided leptin will work perfectly well in the post absorptive (low triglyceride) period? I am a human, not a mouse. I ate a high fat meal without sugar last night, ergo I'm not hungry today. Low trigs equal leptin sensitivity...
I'll call a halt there. Life is full of interesting snippets which make sense. They usually come from the sort of people who say insulin detemir does not cross the blood brain barrier.