This article was sent to me by Stan, and it's interesting on many levels. At the most basic is the gross error in the description of the management of diabetes. This is what the article says:
"In diabetic people, chronic insulin resistance means having to carefully control blood glucose, usually with a diet low in sugar, to avoid a variety of medical complications."
NO NO NO NO NO!
Human diabetes is managed by a diet low in FAT. Ask any diabetologist.
The experience of Dr Dahlqvist encapsulates the monstrous medical approach to the use of low carbohydrate diets in diabetes.
I'm feeling a bit polite tonight for some reason so I won't mention what I think about low fat diets and diabetets. Perhaps I need a glass of wine.
This marine mammal researcher can see physiological insulin resistance in dolphins and see that it is PHYSIOLOGICAL. The difference between a healthy dolphin and a healthy human is minimal (can she see that too?). We humans "do" physiological insulin resistance. But she and her collaborators cannot see that there is a difference between physiological insulin resistance and breaking your liver by living on soda and bagels to get pathological insulin resistance... As she says:
"If we started feeding dolphins Twinkies, they would have diabetes."
Not true. Their insulin resistance would go as they switched on carbohydrate metabolism in their muscles. It would take several years of Twinkies to cause diabetes. Like humans. We're fine for the first few hundred/thousand Twinkies. Then we break.
EDIT: Being in the UK I hadn't realised how small Twinkies are. Let's say 100,000 or so to break your liver...
But ultimately we humans need Twinkies to survive. We must eat them to remain happy and feel part of normal society. Imagine a teenager saying no to a Twinkie, just because they are diabetic! No, we must help people to eat Twinkies while diabetic, so we MUST research the "fasting gene" which is abnormally activated in human diabetes. And develop a drug to turn it off, of course.
BTW the activator of the fasting gene will turn out to be palmitic acid. What other messenger would you use to suggest that there is a fasting state? So we're back to using Palmitofake and a continuous supply of Twinkies.
The title says "Dolphins have diabetes off switch"
No, they do not. There is no off switch for a broken liver. Unbroken dolphins are just behaving like unbroken humans. They turn off physiological insulin resistance when carbohydrate becomes available, even if that carbohydrate come from fish via gluconeogenesis. It's simple and it's NOT diabetes.
Sigh.
Peter
There is potentially a whole load more posts from this link, follow up depends on all sorts of things...
It's not just diabetics that shouldn't have to live without cake. Going by what I see in the market these days, Celiacs shouldn't either.
ReplyDeleteObviously those dolphins would be much better off if they spent 45 minutes ever day on a treadmill.
Bravo, Peter.. dolphins do have an advantage over us.. no USDA or ADA to help them develop diabetes.
ReplyDeletehttp://jeb.biologists.org/cgi/content/full/211/18/2943
ReplyDeleteJust another piece of the puzzle.
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Hormonal regulation of glucose clearance in lactating northern elephant seals (Mirounga angustirostris)
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Glucagon levels in fasting and lactating elephant seals remain stable (Champagne et al., 2006; McDonald, 2003), in contrast to weanling elephant seals, which exhibit an increase in glucagon across the fasting period (Champagne et al., 2005; Ortiz et al., 2003). Basal glucagon levels are lower in fasting elephant seals than in other species during fasting (Fery et al., 1990) and lactation (Burnol et al., 1983; Tigas et al., 2002). While glucagon has been shown to increase with fasting duration in humans (Boyle et al., 1989; Fery et al., 1990), humans that are fasting and lactating simultaneously have stable glucagon levels (Tigas et al., 2002). Glucagon is stable across lactation in cattle, rats and sheep (Burnol et al., 1983; Sartin et al., 1985; Vernon and Pond, 1997). Glucagon stimulates both gluconeogenesis and lipolysis (Perea et al., 1995). Low levels of glucagon are puzzling in light of high levels of lipolysis and gluconeogenesis but probably contribute to protein sparing.
Studies of carnivore glucose metabolism in the context of lactation are rare. We would expect that the lower carbohydrate diet of carnivores would have important impacts on glucose metabolism; however, some studies do suggest that the high protein diet of carnivores may be associated with impaired ability for glucose clearance. Penguins (Chieri et al., 1972), barn owls (Myers and Klasing, 1999), rainbow trout (Palmer and Ryman, 1972), white sturgeon (Hung, 1991) and American alligators (Coulson and Hernandez, 1983) exhibited reduced glucose clearance when compared to omnivores. We are aware of no similar studies in wild mammalian carnivores.
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I leave it to wiser heads to work this into an eventual cure for diabetes.
Chainey, I wonder if they are doing OGTTs on them? Sports drinks will be next. They already get iron overload in zoos, I don't think we know about in the wild...
ReplyDeleteHi ToddBS, wow! Then we could feed them Twinkies and they wouldn't need to feel socially excluded from the spectators!
HI Ellenwyo, I guess they're OK until they get caught...
donny, that's a bit complex for me too but it looks like most carniovores do insulin resistance. I'm a bit surprised that omnivores don't, but the shuttling back and forth between fasting and lactation without mentioning insulin makes it hard to follow!
Wild dolphins have random BGs around 100mg/dl, range 66 to about 120 max. Under extreme capture stress. That does not strike me as hyperglycaemic and it's another post to try and talk about that. I was wanting to get to photomicrographs of arteriosclerosis but stuff is getting in the way...
Peter
Ha ha ha! Pseudoscience is funny.
ReplyDeleteIndeed, the article’s description of the insulin resistant state of dolphins reminds me of a state of mild ketosis in humans, which many people enter at night, especially if their dinner was low in carbs (or if they had no dinner). Maybe they should have removed the word “diabetic” from: “The overnight changes in their blood chemistry match the changes in [diabetic] humans”.
ReplyDeleteIt seems to me that dolphins have not access to carbs in any significant quantity in their habitat over evolutionary timescales. No fruits, berries, or tubers there, though for all I know maybe sea cucumbers are high carb. ;) How can dolphin lessons be applied to humans?
ReplyDeleteHow timely
ReplyDeleteI was hearing this discussed on NPR radio on Friday, how dolphins had an on/off switch for diabetes and we could study them to design new drugs, blah blah blah...
And I thought to myself, I know exactly what is happening with these dolphins, the discussants are as usual conflating insulin resistance with diabetes.
I was going to search for this article but got sidetracked by other topics.
Thanks to you and Stan for finding it for me.
I'm glad I already knew about your sense of humor or I would have been horribly confused by this blog entry! You were really on a roll with this one, thanks for the laughs!
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ReplyDeleteRecurrent obesity is beneficial in nature, as due to extensive fat depots, obese mammals can prolong phase II of fasting with stimulated fat oxidation and protein conservation, permitting extended survival during nutritional scarcity (5, 6). Due to finite food resources, wild animals practically never develop persistent obesity with comorbidities, but the situation becomes different under domestication. Thus, although the natural body condition of the European polecat is lean, it has the potential for extensive weight gain and obesity analogous to humans. The high fat-% (40%) of the farmed polecats probably results from excessive and prolonged positive energy balance (18) and limited physical activity (19, 20)—crucial aspects in human obesity, as well. Artificial selection for a large body size (21) may also be a causative factor. To the best of our knowledge, there exist no published data on the body adiposity of wild polecats, but it can be assumed that they would be considerably thinner. In fact, the estimated fat-% of 2 wild-caught males was 9.8% ± 6.5% in winter (Mustonen et al. unpubl. data)
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The body fat content of the American marten (Martes americana) averages <6% (13), but data are scanty for wild specimens of related species (14). This natural leanness can be lost in captivity, resembling the sedentary lifestyle of a significant part of the general population with overabundance of high-fat and high-carbohydrate foods and restricted exercise.
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Those are both from here;
http://ebm.rsmjournals.com/cgi/content/full/234/11/1287
If they can't even admit that there might be something special about carbohydrate metabolism that makes it particularly fattening in carnivores, besides just the calories, is there any hope?
Years ago, my roommate had a ferret. The thing was a blur. I couldn't see it becoming inactive unless something ruined its metabolism first.
"The high fat-% (40%) of the farmed polecats probably results from excessive and prolonged positive energy balance"
ReplyDeleteI'm starting to wonder if these guys are even technically sentient. How did they get so fat? Well, I reckon they must have accumulated all that fat. Of course! Why didn't I think of that?
donny:
ReplyDelete"In conclusion, prolonged positive energy balance and restricted physical activity are the key factors leading to excessive obesity in captive polecats, similar to humans."
Translation: When you feed an absolute carnivore on total crap, it gets fat. When you do the same to a human, they write total garbage (and get fat)!
Peter
Hi StephenB,
ReplyDeleteSorry, missed this one. I thing we are looking at basic survival related essential physiological processes here. I'm very willing to give a lot more credence to rat/doplphin studies than many LC bloggers as I'm looking for basic principles, with an eye to species specifics.
There are a couple of oddities about humans but generally we're just animals... Actually, having a well developed diving reflex is one oddity!
Peter