Liittynyt: 2004-05-20 06:07:25
"... asidoketoosin mukahoito homeopaattisella määrällä glukoosia..."
Kiitos hoover, mirka ja ilkka (tämä olisi jäänyt varmaan muuten lukematta)
Js siltä varalta, että joku muukin haluaisi lukea, miten "Atkinssin aiheuttama ketoasidoosi" ammutaan alas kokeellisesti, muttei huomannut sitä tuolta, niin laitan tähän koko sen Phinneyn vastauksen:
Vastaus Lancetin Atkins-juttuun (Chen & al.)
http://livinlavidalocarb.blogspot.com/2 ... s-any.html
3-20-06 UPDATE: I received a response for Dr. Lessnau regarding "any alternative explanation" for his patient's ketoacidosis from a three-decades long physician today:
For starters, I applaud Dr. Lessnau for bringing this interesting case up for discussion. That said, however, Dr. Lessnau seems a bit too eager to blame carbohydrate restriction for his patient's metabolic acidosis. With apologies for my rather formal style, here's why I think he shot from the hip.
In the Lancet case report, Chen and Lessnau (see ref 1 below) suggest that a carbohydrate-restricted diet can induce ketoacidosis in a non-diabetic patient, but the data presented do not support this conclusion.
First: the reported anion gap of 26 represents a 12 mM anion excess above the upper limit of normal. The serum beta-hydroxybutyrate (the dominant circulating ketone moiety in humans), reported at 390 ug/mL, translates to a concentration of 3.7 mM. That is, the ketones in this case (both beta-hydroxybutyrate and acetoacetate) account for only about a third of the apparent anion excess. Thus the ketonemia in this case represents only a minor fraction of the anion excess, and thus is not the primary factor in the reported metabolic acidosis.
Second: the normal physiologic state of nutritional ketosis, also called starvation ketosis, is associated with serum ketones in the 1-5 mM range (as in this case), and this is not normally associated with metabolic acidosis (see refs 2,3,4). So given that nutritional ketosis does not cause acidosis despite up to 5 millimolar ketones, how is it credible to blame 4 millimoles of ketones for a 12 millimolar of excess anions in this case?
Third: in their case report, Dr. Lessnau states that they provided the patient with dextrose at the rate of only 38 g/d (5% dextrose at 30 ml/hr). This is not enough carbohydrate to reverse nutritional ketosis, and yet the patient improved. If the ketogenic state was the cause of her problem, why did it improve on a homeopathic dose of glucose?
Fourth: Yes, a barcarbonate of 8 and an anion gap of 26 are worrisome, and any ER doc would admit this patient for evaluation and rehydration. However most of us would save the term "severe acidosis" for anion gaps greater than 30 and blood pH values under 7.1. Calling an arterial blood pH of 7.19 "severe acidosis" is a bit of hyperbole.
Fifth: patients with pancreatitis can have an elevate lipase but normal serum amylase (see ref 5). Given her elevated lipase, white blood cell count of 13x10.ninth, and gastrointestinal symptoms, why was this not just a case of mild pancreatitis? We all know that CT scans of the abdomen in someone with a BMI of 41 are notoriously difficult to interpret for soft-tissue injury.
Sixth: I agree with Science4u1959 in questioning the frequency of events such as this case during low carbohydrate dieting. As an academic physician with 30 years of experience in adult weight management, I have not seen a similar case in over 3000 patients followed closely during a very low calorie ketogenic diet. Given this experience, I think that it is likely that the current case represents association without causality. Not having this experience, it is unfortunate that Dr. Lessnau chose to conclude causality rather than raising it as a hypothesis.
Stephen D. Phinney, MD, PhD
Professor emeritus, UC Davis
Elk Grove, CA, USA
1. Chen TY, Smith W, Rosenstock JL, Lessnau KD. A life-threatening complication of Atkins diet. The Lancet 2006;367:958.
2. Cahill GF. Starvation in man. N Engl J Med 1970; 282:668-675.
3. Phinney SD, Horton ES, Sims EAH, Hanson JS, Danforth E, LaGrange BM. Capacity of moderate exercise in obese subjects after adaptation to a hypocaloric, ketogenic diet. J Clin Invest. 1980;66:1152-1161.
4. Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL. The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation. Metabolism 1983; 32:757–768.
5. Sharma P, Lim S, James D, Orchard RT, Horne M, Seymour CA. Pancreatitis may occur with a normal amylase concentration in hypertriglyceridaemia
Erkki terveys- eko- ja eettisistä syistä. Tyyli täällä, kliks
Ei eläinkään pysy terveenä jatkuvasti vaihtelevalla sapuskalla.We are 90% microbes and 10% human.
Why invent a cure when you can profit from thousands of remedies? (DrWho)