question re:Ketosis

[thebabydoc]

I'm kind of embarassed to ask this, being a doctor, but what exactly is the theory behind putting one's body into ketosis? I tried the ketogenic diet for like 3 weeks and it helped me to learn how to kick carbs but otherwise was just painful. I read that the rebound storage of fat is scary with this kind of a diet.

The "Zone", on the other hand has been unbelievable for me; I'm a true convert.

 

[Mr.X]

I'm kind of embarassed to ask this, being a doctor, but what exactly is the theory behind putting one's body into ketosis? I tried the ketogenic diet for like 3 weeks and it helped me to learn how to kick carbs but otherwise was just painful. I read that the rebound storage of fat is scary with this kind of a diet.

The "Zone", on the other hand has been unbelievable for me; I'm a true convert.

Theory (reality for that matter) is simple...when you enter the state of Ketosis your body basically switches from burning carbohydrates for fuel to burning fat for fuel. The main concern for you and Ketosis (you being a doctor) is KetoAcidosis: ketones are the end result of "incomplete" breakdown of fats, with the ketones being the "remnants, ash, etc." left over from this. Ketoacidosis IS dangerous in a diabetic, no question about it. Ketoacidosis however IS NOT dangerous in normal healthy humans adapting a high fat/protein, low carb diet. Acidosis simply means an increased amount of acid in the blood. Ketone bodies are acids and therefore CAUSE acidosis. Aftert a short period of time 3-5 days, the blood PH levels are usually stabilize to neutral.

Ketosis (low-carbs) can have a big effect on overall bodyfat, and research has documented this effect. In one study of ideal-weight human subjects, it was found that high fat diets were accompanied by a very strong lipolytic (fat burning) effect. (ref 1)
Kather H, Wieland E, Scheurer A, et al. Influences of variation in total energy intake and dietary consumption on regulation of fat cell lipolysis in ideal weight subjects. J Clin Invest 1987; 80(2):556-72.

P.S. Read
www.elitefitness.com/articles
Mr.X dieters digest for futher info
Mr.X

 

[thebabydoc]

thanks alot, X

good info

so would that mean that modifying a "zone" diet from 30-30-40 to say 40% fat would be even better?
Also, my understanding is that ketones are not a good source for glucose which the brain needs for efficient activity,
how does the body get around this?

 

[diamonddiceclay]

the brain functions fine especially if you eat 1 day a week of high carbs to balance the diet

 

[Mr.X]

thanks alot, X

good info

so would that mean that modifying a "zone" diet from 30-30-40 to say 40% fat would be even better?
Also, my understanding is that ketones are not a good source for glucose which the brain needs for efficient activity,
how does the body get around this?

I think if you modify it to 40% and doing that you add EFA's (healthy fats) then you're probably going to see quiet better results. Here's something that might help you w/ the glucose/brain problem.

Diet-induced ketosis increases monocarboxylate transporter (MCT1) levels in rat brain.

Leino RL, Gerhart DZ, Duelli R, Enerson BE, Drewes LR.

Department of Anatomy and Cell Biology, School of Medicine, University of Minnesota, Duluth, MN 55812, USA.

Monocarboxylate transporter (MCT1) levels in brains of adult Long-Evans rats on a high-fat (ketogenic) diet were investigated using light and electron microscopic immunocytochemical methods. Rats given the ketogenic diet (91% fat and 9% protein) for up to 6 weeks had increased levels of the monocarboxylate transporter MCT1 (and of the glucose transporter GLUT1) in brain endothelial cells and neuropil compared to rats on a standard diet. In ketonemic rats, electron microscopic immunogold methods revealed an 8-fold greater MCT1 labeling in the brain endothelial cells at 4 weeks. Abluminal endothelial membranes were twice as heavily labeled as luminal membranes. In controls, luminal and abluminal labeling was not significantly different. The endothelial cytoplasmic compartment was sparsely labeled (<8% of total endothelial labeling) in all brains. Neuropil MCT1 staining was more intense throughout the brain in ketonemic rats, especially in neuropil of the molecular layer of the cerebellum, as revealed by avidin-biotin immunocytochemistry. This study demonstrates that adult rats retain the capacity to upregulate brain MCT1 levels. Furthermore, their brains react to a diet that increases monocarboxylate levels in the blood by enhancing their capability to take up both monocarboxylates (MCT1 upregulation) and glucose (GLUT1 upregulation). This may have important implications for delivery of fuel to the brain under stressful and pathological conditions, such as epilepsy and GLUT1 deficiency syndrome.

PMID: 11248400 [PubMed - indexed for MEDLINE]

Mr.X