Question about Atkins

[desi]

Well, the principles of sound dietary practice are based on science, which is based on observed evidence, from which we draw conclusions. One of the basic premises is critical review, and peer review generally does this pretty well.

In short, I have been asking you to provide references. The fact that you cannot speaks volumes.

Now I'm asking you to provide references in support of the Atkins diet. Give me reference to a double-blind placebo controlled study funded by an independent source whose results suggest the Atkins diet is effective and less harmful than other diets. Well? Lets hear it Catalyst.

 

[catalyst]

How do you show something to be less harmful? Furthermore, you are shifting the burdren of proof. However, I will show you references that ketogenic diets are effective, and used in a variety of methods to treat quite a few conditions, in addition to the normal dietary goal of fat loss.

 

[catalyst]

References for ketogenic diet:



Berry-Kravis E, Booth G, Sanchez AC, Woodbury-Kolb J. Carnitine levels and the

ketogenic diet. Epilepsia 2001;42(11):1445-1451.

Carroll J, Koenisberger D. The ketogenic diet: A practical guide for caregivers. J Am

Diet Assoc 1998;98(3):316-321.

Couch SC, Schwarzman F, Carroll J, Koenigsberger D, Nordli DR, Deckelbaum RJ,

DeFelice AR. Growth and nutritional outcomes of children treated with the ketogenic

diet. J Am Diet Assoc 1999;99(12)1573-1575.

DiMario FJ Jr, Holland J. The ketogenic diet: a review of the experience at Connecticut

Children’s Medical Center. Pediatr Neurol 2002;26(4):288-292.

Freeman JM, Freeman JB, Kelly MT. The Ketogenic Diet: A Treatment for Epilepsy.

3rd ed. Demos Medical Publishing, New York, NY; 2000.

Freeman JM, Vining EP. Seizures decrease rapidly after fasting: preliminary studies of

the ketogenic diet. Arch Pediatr Adolesc Med 1999;153(9):946-949.

Gilbert DL, Pyzik PL, Vining EP, Freeman. Medication cost reduction in children on the

ketogenic diet: data from a prospective study. J Child Neurol 1999;14(7):469-471.

Hassan AM, Keene DL, Whiting SE, Jacob PJ, Champagne JR, Humphreys P. Ketogenic

diet in the treatment of refractory epilepsy in childhood. Pediatr Neurol 1999;21(2)548-

552.

Hemingway C, Freeman JM, Pillas DJ, Pyzik PL. The ketogenic diet: A 3- to 6- year

follow-up on 150 children enrolled prospectively. Pediatr 2001;108(4):898-905.

Howrie DL, Kraisinger M, McGhee HW, Crimrine PK, Katyal N. The ketogenic diet:

The need for a multidisciplinary approach. Ann Pharmaco 1998;32:384-384.

Katyal NG, Koehler AN, McGhee B, Foley CM, Crumrine PK. The ketogenic diet in

refractory epilepsy: The experience of Children’s Hospital of Pittsburgh. Clin Pediatr

2000;39:153-159.

Kossoff EH, Pyzik PL, McGrogan JR, Vining EPG, Freeman JM. Efficacy of the

ketogenic diet for infantile spasms. Pediatr 2002;109(5)780-783.

Page 2

Lefevre F, Aronson N. Ketogenic diet for the treatment of refractory epilepsy in

children: a systematic review of efficacy. Pediatr 2000;105(4).URL:

http://www.pediatrics.org/cgi/content/full/105/4/e46.

MacCracken KA, Scalisi JC. Development and evaluation of a ketogenic diet program. J

Am Diet Assoc 1999;99(12)1554-1558.

Mandel A, Ballew M, Pina-Garza JE, Stalmasek V, Clemens LH. Medical costs are

reduced when children with intractable epilepsy are successfully treated with the

ketogenic diet. J Am Diet Assoc 2002;102(3):396-398.

Nordli DR, Kuroda MM, Carroll J, Koenisberger DY, Hirsch LJ, Bruner HJ, Siedel WT,

De Vivo DC. Experience with the ketogenic diet in infants. Pediatr 2001;108(1):129-

133.

Pulsifer MB, Gordon JM, Vining EPG, Freeman JM. Effects of ketogenic diet on

development and behavior: preliminary report of a prospective study. Dev Med Child

Neuro 2001;43:301-306.



Tallian KB, Nahata MC, Tsao C-Y. Role of the ketogenic diet in children with

intractable seizures. Ann Pharmaco 1998;32:349-361.

Wheless JW. The ketogenic diet: An effective medical therapy with side effects. J Child

Neuro 2001;16(9):633-635.

Williams S, Basualdo-Hammond C, Curtis R, Schuller R. Growth retardation in children

with epilepsy on the ketogenic diet: A retrospective chart review. J Am Diet Assoc.

2002;102(3):405-407.



· Lennox WG. Ketogenic diet in the treatment of epilepsy. N Engl J Med 199:74-75 1928.

· Huttenlocher PR. Ketonemia and seizures: metabolic and anticonvulsant effects of two ketogenic diets in childhood epilepsy. Pediatric Res 31:152-60 1976.

· Schwartz RM, Eaton J, Bower BD, Aynsley-Green A. Ketogenic diets in the treatment of epilepsy: short term clinical effects. Dev Med Child Neurol 31:145-51 1989.

· Vining EPG, Freeman JM, Ballaban-Gil K, Camfield CS, Camfield PR, Holmes GL, Shinnar S, Shuman R, Trevathan E, Wheless JW and the Ketogenic Diet Multi-Center Study Group. A multicenter study of the efficacy of the ketogneic diet. Arch Neurol 55:1433-1437 1998.

· Sirven J, Whedon B, Caplan D, Liporace J, Glosser D, O'Dwyer J, Sperling MR. The ketogenic diet for intractable epilepsy in adults: preliminary results. Epilepsia 40:1721-1726 1999.

· Schwartzkroin PA. Mechanisms underlying the antipepileptic efficacy of the ketogenic diet. Epilepsy Research 37:151-180 1999.

· Ge S and Niesen C. BHB potentiates GABA-A mediated inhibitory post-synaptic potentials in immature hippocampal CA1 neurons. Epilepsia 39: Supplement 6 E.06 1998.

· Voskuyl RA, Vreugdenhil M, Kang JX, Leaf A. Anticonvulsant effect of ppolyunstaurated fatty acids in rats, using the cortical simulation model. Eur J Pharm 341:145-152 1998.

· Devivo DC, Leckie MP,l Ferrendelli JS, McDougal DB. Chronic ketosis and cerebral metabolism. Ann Neurol 3:331-337 1978



· Hasselbalch SG, Madsen PL, Hageman LP, Olsen KS, Justesen N, Holm S, Paulson OB. Changes in cerebral blood flow and carbohydrate metabolism during acute hyperketonemia. Am J. Physio 270:E746-751 1996.

· Owen OW, Morgan AP, Kemp HG, Sullivan JM, Herrera MG, Cahill GF. Brain metabolism during fasting. J Clin Inv 4:1589-1595 1967



Balasse, EO and F. Fery. "Ketone body production and disposal: effects of fasting, diabetes, and exercise. [Review]" Diabetes - Metabolism Reviews 5(3): 247-70, 1989.

Biolo G. et. al. "Physiologic hyperinsulinemia stimulates protein synthesis and enhances transport of selected amino acids in human skeletal muscle." J Clin Investigation 95(2): 811-9, 1995.

Cutler, D.L. "Low-carbohydrate diet alters intracellular glucose metabolism but not overall glucose disposal in exercise-trained subjects." Metabolism: Clinical and Experimental 44(10): 1364-70, 1995.

John M. Freeman, Kelly, M. and Freeman, Jennifer. The epilepsy diet treatment: an introduction to the ketogenic diet. Freeman, Kelly, Freeman, 1994.

Fery, F. and EO Balasse "Response of ketone body metabolism to exercise during transition from postabsorptive to fasted state." Am J Physiology 250 (5 Pt 1): E495-501, 1986.

Haussinger D. "Control of protein turnover by the cellular hydration state." [Review] Italian J Gastroenterology 25(1): 42-8, 1993.

Haussinger D. et. al. "Cellular hydration state: an important determinant of protein catabolism in health and disease." Lancet 341 (8856): 1330-2, 1993.

Henriksson, J. "Influence of exercise on insulin sensitivity. [Review]" J Cardiovascular Risk. 2(4): 303-9, 1995.

Kather, H. et. al. "Influences of variation in total energy intake and dietary composition on regulation of fat cell lipolysis in ideal-weight subjects." J Clin Investigation. 80(2): 566-72, 1987.

Lambert EV et. al. "Enhanced endurance in trained cyclists during moderate intensity exercise following 2 weeks adaptation to a high fat diet." Eur J App Physiology & Occup Physiology 69(4): 287-93, 1994.

Mitchell GA et al. "Medical aspects of ketone body metabolism. [Review]" Clinical & Investigative Medicine 18(3): 193-216.

Phinney SD. et. al. "The human metabolic response to chronic ketosis without caloric restriction: preservation of submaximal exercise capacity with reduced carbohydrate oxidation." Metabolism: Clinical & Experimental 32(8): 769-76, 1983.

Phinney SD. et. al. "The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation." Metabolism: Clinical & Experimental 32(8): 757-68, 1983.

Sidery, MB. et. al. "The initial physiological responses to glucose ingestion in normal subjects are modified by a 3 d high-fat diet." British J Nutrition 64(3): 705-13, 1990.

Wing RR, et. al. "Cognitive effects of ketogenic weight-reducing diets." Int J Obesity & Related Metabolic Disorders 19(11): 811-6, 1995.



· "The John Hopkins Ketogenic Diet Fact Sheet." Epilepsy Foundation of America. 4351 Garden City Drive. Landover, MD 20785-2267.


· An introduction to the ketogenic diet: A treatment for pediatric epilepsy [video-recording]. Santa Monica (CA): Charlie Foundation To Help Cure Pediatric Epilepsy, 1994.

· Schwartz RM, Boyes S, Aynsley-Green A, Metabolic effects of three ketogenic diets in the treatment of severe epilepsy. Dev Med Child Neurol 1989: 31(2): 152-60.

· Haymond MW, Howard C, Ben-Galim E, DeVivo DC. Effects of ketosis on glucose flux in children and adults. Am J Physiol 1983: 245(4): E373-8.

· Huttenlocher PR, Wilbourn AJ, Signore JM. Medium-chain triglycerides as a therapy for intractable childhood epilepsy. Neurology 1971: 21: 1097-1103.

 

[catalyst]

Foster GD, Wyatt HR, Hill JO, McGuckin BG, Brill C, Mohammed BS, Szapary PO, Rader DJ, Edman JS, Klein, S. A Multicenter, Randomized, Controlled Trial of a Low-Carbohydrate Diet for Obesity. New England Journal of Medicine, vol. 348:21, pp. 2082-2090, May 12, 2003.

This is a very good study, and it shows that "researchers have found that at three and six months, the Atkins’ diet produces significantly greater weight loss than a conventional low-fat, high-carbohydrate diet."

 

[catalyst]

While I am at it, studies showing the negative effects of low-fat dieting (mainly lowering testosterone levels). For those who think that this is not significant, testoserone is required to not only build, but maintain muscle tissue, and a drop in test levels decreases the ability to do this, which means greater muscle catabolism, which leads to a decrease in the basal metabolic rate.

[font=verdana, arial, helvetica] J Steroid Biochem. 1984 Jan;20(1):459-64.
Diet and serum sex hormones in healthy men.

Hamalainen E, Adlercreutz H, Puska P, Pietinen P.

The possible effect of dietary fat content and the ratio of polyunsaturated to saturated fatty acids (P/S-ratio) on serum sex hormones was studied in 30 healthy male volunteers. The customary diet of the subjects, which supplied 40% of energy as fat (mainly from animal sources, P/S-ratio 0.15) was replaced for a 6 weeks period by a practically isocaloric experimental diet containing significantly less fat (25% of energy) with a higher P/S-ratio (1.22) and other environmental factors were stabilized. Serum testosterone and 4-androstenedione decreased from 22.7 +/- 1.1 nmol/l to 19.3 +/- 1.2 nmol/l, (SEM, P less than 0.001) and from 4.6 +/- 0.2 nmol/l to 4.3 +/- 0.2 nmol/l (SEM, P less than 0.01), respectively. These changes were paralleled by a reduction in serum free (non-protein bound) testosterone (P less than 0.01) suggesting a possible change in biological activity. During the low fat period a significant negative correlation between serum prolactin and androgens was observed. All the changes in androgen levels were reversible. With the exception of a small but non-significant decrease in serum estradiol-17 beta, the other hormone parameters were practically unaffected by the dietary manipulation. Our results indicate that in men a decrease in dietary fat content and an increase in the degree of unsaturation of fatty acids reduces the serum concentrations of androstenedione, testosterone and free testosterone. The mechanism and importance of this phenomenon is discussed in the light of epidemiological and experimental data.


J Steroid Biochem. 1983 Mar;18(3):369-70.

Decrease of serum total and free testosterone during a low-fat high-fibre diet.

Hamalainen EK, Adlercreutz H, Puska P, Pietinen P.

The concentrations of serum total and free testosterone were studied in 30 healthy, middle-aged men during a dietary intervention program. When men were transferred from their customary diet to an experimental diet, which contained less fat with a higher polyunsaturated/saturated ratio (P/S-ratio) and more fibre, there was a significant decrease in serum total testosterone concentrations (22.7 +/- 1.2 vs 19.3 +/- 1.1 nmol/l SEM, P less than 0.001). Furthermore, serum free, unbound testosterone fell from 0.23 +/- 0.01 to 0.20 +/- 0.01 nmol/l SEM (P less than 0.01). The hormonal changes were reversible. This observation suggests that testosterone activity in plasma can at least partly be modified by changing the composition of the diet.


Am J Clin Nutr. 1996 Dec;64(6):850-5.

Effects of dietary fat and fiber on plasma and urine androgens and estrogens in men: a controlled feeding study.

Dorgan JF, Judd JT, Longcope C, Brown C, Schatzkin A, Clevidence BA, Campbell WS, Nair PP, Franz C, Kahle L, Taylor PR.

Division of Cancer Prevention and Control, National Cancer Institute, Bethesda, MD 20892-7326, USA. dorganj@dcpcepn.nci.nih.gov

We conducted a controlled feeding study to evaluate the effects of fat and fiber consumption on plasma and urine sex hormones in men. The study had a crossover design and included 43 healthy men aged 19-56 y. Men were initially randomly assigned to either a low-fat, high-fiber or high-fat, low-fiber diet for 10 wk and after a 2-wk washout period crossed over to the other diet. The energy content of diets was varied to maintain constant body weight but averaged approximately 13.3 MJ (3170 kcal)/d on both diets. The low-fat diet provided 18.8% of energy from fat with a ratio of polyunsaturated to saturated fat (P:S) of 1.3, whereas the high-fat diet provided 41.0% of energy from fat with a P:S of 0.6. Total dietary fiber consumption from the low- and high-fat diets averaged 4.6 and 2.0 g.MJ-1.d-1, respectively. Mean plasma concentrations of total and sex-hormone-binding-globulin (SHBG)-bound testosterone were 13% and 15% higher, respectively, on the high-fat, low-fiber diet and the difference from the low-fat, high-fiber diet was significant for the SHBG-bound fraction (P = 0.04). Men's daily urinary excretion of testosterone also was 13% higher with the high-fat, low-fiber diet than with the low-fat, high-fiber diet (P = 0.01). Conversely, their urinary excretion of estradiol and estrone and their 2-hydroxy metabolites were 12-28% lower with the high-fat, low-fiber diet (P < or = 0.01). Results of this study suggest that diet may alter endogenous sex hormone metabolism in men.[/font]

 

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Some references for the importance of obtaining essential fatty acids, which is difficult to do on a low fat diet. For those who think "Well, I can just supplment", this is true. Just like a ketogenic diet is often low in calcium. Any diet will create a deficiency, which is one of the many points that I have made which has been ignored by at least one person.

[font=verdana, arial, helvetica]PREVENTION OF SUDDEN DEATH BY LOW INTAKES OF N-3 POLYUNSATURATED FA



David Siscovick

University of Washington, Seattle, WA, USA



There is mounting evidence that modest dietary intake of fatty fish and low-dose, long-chain, n-3 polyunsaturated fatty acid (PUFA) supplementation are associated with a reduced risk of out-of-hospital primary cardiac arrest, also known as sudden cardiac death. In contrast, modest intake of long-chain w3 PUFAs is not associated with a reduced risk of non-fatal myocardial infarction. In this presentation, we discuss the potential role of modest intake of w3 PUFAs in the prevention of sudden cardiac death in the community. We suggest that differences in the findings from prior epidemiologic studies of fish and long-chain w3 PUFA intake and the risk of coronary heart disease may relate to differences in the primary focus of the research, the distribution of long-chain w3 PUFA intake and other dietary FA in the population, and the outcomes examined. We illustrate these issues with data from a population-based case-control study of dietary intake and cell-membrane levels of long-chain w3 PUFAs and the risk of primary cardiac arrest. Prior research has not examined whether modest dietary intake of fatty fish or low-dose w3 PUFA supplementation is associated with a reduced risk of sudden cardiac death and/or non-fatal myocardial infarction in patients with type II diabetes mellitus. Based upon evidence from epidemiologic studies and clinical trials, we suggest several methodological issues that should be considered in the design of a clinical trial to examine the effects of modest intake of long-chain w3 PUFAs on cardiovascular outcomes among patients with type II diabetes mellitus.

EFFECTS OF w3 FA ON BLOOD PRESSURE



Trevor A Mori

University of Western Australia and the West Australian Heart Research Institute

Perth, Western Australia, Australia



In recent studies in humans we have shown significant benefits of w3 fatty acids on blood pressure (BP). The first, was a randomised, controlled trial examining the independent and combined effects of dietary fish and weight-loss on 24hr ambulatory BP in 63 treated, overweight hypertensives, for 16-wks. Fish and weight-loss had significant independent and additive effects on 24hr ambulatory BP. The second study, examined the independent effects of EPA or DHA, using a double-blind, randomised, placebo-controlled parallel design. Fifty-six mildly hyperlipidaemic but otherwise healthy men, took 4g daily of purified EPA, DHA, or olive oil capsules for 6 weeks. DHA, but not EPA, reduced 24hr and awake ambulatory BP. We have demonstrated that a daily fish meal as part of a reduced-fat diet, had additive effects on BP reduction in obese treated hypertensives. Furthermore, DHA, but not EPA, significantly reduced ambulatory BP. Thus, DHA may be the principal w3 fatty acid that lowers BP in humans.

MODULATION OF ENDOTHELIAL HEALTH BY w3 FATTY ACIDS



Gary McVeigh

Queen's University of Belfast, Ireland



Omega-3-FA favorably influence many of the mechanisms involved in atherogenesis and may reduce mortality from coronary heart disease. We found that dietary supplementation with omega-3-FA improved endothelium-dependent responses to the infusion of acetylcholine into the brachial artery. These responses were accompanied by improved compliance characteristics of the arterial circulation. These data support the hypothesis that the direct vascular effects of omega-3-fatty acids on arterial reactivity and wall characteristics may contribute to their cardioprotective actions in humans.


EFFECTS OF w3 FATTY ACIDS ON LDL-CHOLESTEROL IN DIABETIC PATIENTS



William S. Harris

Mid America Heart Institute, Kansas City, MO, USA



Fish oils rich in marine w3 FA have clear effects on serum lipid and lipoprotein levels. When consumed in relatively large doses (i.e., 3-6 g/d), w3 FA reduce fasting triglyceride levels by 20-40%. However, at lower intakes (i.e., 1 g/d), minimal effects are noted. Similarly, at high doses, LDL-C levels often rise 10-20% (especially in the short-term and in hypertriglyceridemic patients), but not at lower intakes. Although these findings have largely come from studies In non-diabetic patients, current evidence suggests that the same is true in type 2 diabetes. In 14 data sets taken from placebo-controlled, randomized trials in patients with type 2 diabetes, an average of 3.7 g of w3 FA was given per day. The mean triglyceride decrease was 33%, and the decrease was statistically significant in every study. LDL-C levels increased an average of 10%, but in only 3 data sets were the increases statistically significant. When considering the effects of low intakes of w3 FA on LDL-C, no studies have yet been reported in diabetic subjects. In non-diabetic subjects, intakes of 2 g or less have produced a 3% increase in LDL-C on average, similar to that seen in the GISSI Prevenzione study. Thus, both moderate (3-4 g) and low (<2 g) low w3 FA intakes have a minor impact on LDL-C levels. Whether this is clinically significant is unclear, but the positive results of several clinical trials focusing on total mortality would argue that the impact is negligible.


CAN OMEGA-3 FA IMPROVE HEART RATE VARIABILITY?



Erik Berg Schmidt

Aalborg Hospital, Aalborg, Denmark



Heart rate variability (HRV), a measure of cardiac autonomic nerve balance, is associated with a reduced risk of sudden cardiac death. We have studied the association between fish consumption, cellular levels of omega-3 FA and HRV, measured by 24-hour Holter monitoring. We have studied healthy subjects, patients with CHD, patients with diabetes mellitus and patients on hemodialysis. We have undertaken intervention studies with fish oils in patients with CHD, renal disorders and healthy volunteers. We conclude that fish consumption, cellular levels of omega-3 FA (in particular DHA) and fish oil supplementation are positively associated with HRV. This suggests that marine omega-3 FA may decrease the risk of sudden cardiac death.


EVOLUTIONARY ASPECTS OF OMEGA-3 FATTY ACID INTAKE



Artemis P. Simopoulos

The Center for Genetics, Nutrition and Health, Washington, D.C., USA



Studies on the evolutionary aspects of diet indicate that major changes have taken place in our physical activity and diet, particularly in the type and amount of essential FA (w6 and w3) and antioxidant intake. Assuming 35% of energy came from animals and 65% from plants, the estimated intake of essential FA from animal and vegetable sources in the Late Paleolithic period shows that the ratio of linoleic acid to a-linolenic acid (LA:ALA) is 0.70, whereas the ratio of longer chain w6:w3 is 1.79, giving a ratio of total w6:w3 of 0.79. In the United States, again considering the same subsistence ratio of animal sources to plants sources of 35:65, the current diet would provide a ratio of 16.74, which is close to estimates of 15-20:1 of other investigators. Considering other populations, i.e., in Japan the w6:w3 ratio is 4:1, and in the United Kingdom this ratio is 15:1, whereas 20 years ago it was 10:1. Similar ratios have been suggested for northern Europe and Holland with lower ratios in southern Europe due to higher consumption of olive oil instead of corn and safflower oils. In the past 20 years the ratio changed from 10:1 to 15:1 in England and northern Europe. The shift in the decrease in w3 fatty acid intake is reflected in the declining concentrations of docosahexaenoic acid (DHA) and rising concentrations of LA in human milk. The traditional diet of Greece prior to 1960 had a ratio of 1-2:1. In general, there are a few reliable estimates of the intake of longer chain omega-3 PUFA. The increase in the w6:w3 ratio is a totally new phenomenon in the diet of human beings. Current intake differs from our ancestors’ intake who consumed w6 and w3 FA in roughly equal amounts. Such an enormous change in a short period of time does not allow time for adaptation. The w3 and w6 essential FA are not interconvertible in the human body and are important components of practically all cell membranes. w6 and w3 FA influence eicosanoid metabolism, gene expression, and intracellular cell communication. Because the PUFA composition of cell membranes is to a great extent dependent on dietary intake, appropriate amounts of dietary w6 and w3 FA need to be considered in making dietary recommendations, and these two classes of PUFAs should be distinguished because they are metabolically and functionally distinct and have opposing physiological functions. Their balance is important for homeostasis and normal development. A balanced ow6:w3 ratio in the diet is essential for normal growth and development and should lead to decreases in cardiovascular disease, other chronic diseases and improve mental health.[/font]

 

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[font=verdana, arial, helvetica] J Am Diet Assoc. 1995 Jun;95(6):693-7.
Implementing a ketogenic diet based on medium-chain triglyceride oil in pediatric patients with cancer.

Nebeling LC, Lerner E.

Nutrition Department, Case Western Reserve University, Cleveland, Ohio 44106-4906, USA.

Traditionally, a ketogenic diet is given to drug-resistant children with epilepsy to improve seizure control. Inducing a ketogenic state in patients with cancer may be a useful adjunct to cancer treatment by affecting tumor glucose metabolism and growth while maintaining the patient's nutritional status. A ketogenic diet consisting of 60% medium-chain triglyceride (MCT) oil, 20% protein, 10% carbohydrate, and 10% other dietary fats was provided to a select group of pediatric patients with advanced-stage cancer to test the effects of dietary-induced ketosis on tumor glucose metabolism. Issues of tolerance and compliance for patients consuming an oral diet (consisting of normal table foods and daily MCT oil "shakes") and for patients receiving an enteral formula are reviewed. Preliminary use of the MCT oil-based diet suggests a potential in pediatric patients with cancer.


J Am Coll Nutr. 1995 Apr;14(2):202-8.


Effects of a ketogenic diet on tumor metabolism and nutritional status in pediatric oncology patients: two case reports.

Nebeling LC, Miraldi F, Shurin SB, Lerner E.

Nutrition Department, Case Western Reserve University, School of Medicine, Cleveland, Ohio, USA.

OBJECTIVE: Establish dietary-induced ketosis in pediatric oncology patients to determine if a ketogenic state would decrease glucose availability to certain tumors, thereby potentially impairing tumor metabolism without adversely affecting the patient's overall nutritional status. DESIGN: Case report. SETTING: University Hospitals of Cleveland. SUBJECTS: Two female pediatric patients with advanced stage malignant Astrocytoma tumors. INTERVENTIONS: Patients were followed as outpatients for 8 weeks. Ketosis was maintained by consuming a 60% medium chain triglyceride oil-based diet. MAIN OUTCOME MEASURES: Tumor glucose metabolism was assessed by Positron Emission Tomography (PET), comparing [Fluorine-18] 2-deoxy-2-fluoro-D-glucose (FDG) uptake at the tumor site before and following the trial period. RESULTS: Within 7 days of initiating the ketogenic diet, blood glucose levels declined to low-normal levels and blood ketones were elevated twenty to thirty fold. Results of PET scans indicated a 21.8% average decrease in glucose uptake at the tumor site in both subjects. One patient exhibited significant clinical improvements in mood and new skill development during the study. She continued the ketogenic diet for an additional twelve months, remaining free of disease progression. CONCLUSION: While this diet does not replace conventional antineoplastic treatments, these preliminary results suggest a potential for clinical application which merits further research.

Br J Cancer. 1987 Jul;56(1):39-43.


Reduction of weight loss and tumour size in a cachexia model by a high fat diet.

Tisdale MJ, Brennan RA, Fearon KC.

An attempt has been made to reverse cachexia and to selectively deprive the tumour of metabolic substrates for energy production by feeding a ketogenic regime, since ketone bodies are considered important in maintaining homeostasis during starvation. As a model we have used a transplantable mouse adenocarcinoma of the colon (MAC 16) which produces extensive weight loss without a reduction in food intake. When mice bearing the MAC16 tumour were fed on diets in which up to 80% of the energy was supplied as medium chain triglycerides (MCT) with or without arginine 3-hydroxybutyrate host weight loss was reduced in proportion to the fat content of the diet, and there was also a reduction in the percentage contribution of the tumour to the final body weight. The increase in carcass weight in tumour-bearing mice fed high levels of MCT was attributable to an increase in both the fat and the non-fat carcass mass. Blood levels of free fatty acids (FFA) were significantly reduced by MCT addition. The levels of both acetoacetate and 3-hydroxybutyrate were elevated in mice fed the high fat diets, and tumour-bearing mice fed the normal diet did not show increased plasma levels of ketone bodies over the non-tumour-bearing group despite the loss of carcass lipids. Both blood glucose and plasma insulin levels were reduced in mice bearing the MAC16 tumour and this was not significantly altered by feeding the high fat diets. The elevation in ketone bodies may account for the retention of both the fat and the non-fat carcass mass. This is the first example of an attempt to reverse cachexia by a diet based on metabolic differences between tumour and host tissues, which aims to selectively feed the host at the expense of the tumour.


Br J Cancer. 1988 Nov;58(5):580-3.

A comparison of long-chain triglycerides and medium-chain triglycerides on weight loss and tumour size in a cachexia model.

Tisdale MJ, Brennan RA.

Pharmaceutical Sciences Institute, Aston University, Birmingham, UK.

A comparison has been made between the ability of long-chain triglycerides (LCT) and medium-chain triglycerides (MCT) to prevent weight loss induced by the cachexia-inducing colon adenocarcinoma (MAC16) and to reduce tumour size. There was no difference in calorie consumption or nitrogen intake between the various groups. When compared with a normal control high carbohydrate, low fat diet, animals fed MCT showed a reduced weight loss and a marked reduction in tumour size. In contrast neither weight loss nor tumour size differed significantly from the controls in animals fed the LCT diet. An elevated plasma level of 3-hydroxybuturate was found only in the animals fed the MCT diets. Administration of LCT caused an increase in the plasma level of FFA, which was not observed in the MCT group. These results suggest that diets containing MCT would provide the best ketogenic regime to reverse the weight loss in cancer cachexia with a concomitant reduction in tumour size.[/font]

 

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The Effects of a High-Carbohydrate, High-Protein or Balanced Lunch Upon Later Food Intake and Hunger Ratings
Reference:
Latner, J.D., Schwartz, M., "The Effects of a High-Carbohydrate, High-Protein or Balanced Lunch Upon Later Food Intake and Hunger Ratings," Appetite, 33(1), 1999, pages 119-128.

Summary:
This study analyzed the impact of various midday meals on appetite and subsequent food intake. Three liquid meals—one high in protein, a second high in carbohydrate and the third combining half portions of the first two—were given to 12 female subjects. The women were found to eat 31% more calories at dinner when fed the high-carbohydrate lunch as opposed to the high-protein lunch, and 20% more calories than when consuming the mixed lunch. Subjects also reported greater pre-dinner hunger when fed the high-carbohydrate lunch than when given the high-protein lunch.

Emphasis mine - Catalyst
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[font=verdana, arial, helvetica]A few direct references on the theory and application of ketogenic dieting as a documented medical protocol for treating epileptic children

Pediatr Res. 1976 May;10(5):536-40.

Ketonemia and seizures: metabolic and anticonvulsant effects of two ketogenic diets in childhood epilepsy.

Huttenlocher PR.

Metabolic effects of a new ketogenic regimen in which ketonemia is induced by feeding of medium chain triglycerides (MCT) are described, and comparisons are made with effects of the standard high fat ketogenic diet. Eighteen children maintained on the MCT diet for 3 months to 4 years failed to show elevations of serum cholesterol and had only a slight rise in serum total fatty acids, in contrast to the marked hyperlipidemia observed in children on the standard high fat diet. Long term use of the MCT diet did not affect pH of venous blood. Blood glucose fell below 50 mg/100 ml in one-third of the children, the lowest levels being reached 2--3 weeks after the start of the diet. Plasma D(--)-beta-hydroxybutyrate (BHB) and acetoacetate rose gradually after institution of diet therapy, maximum levels being reached after about 1 month. Higher levels of BHB and acetoacetate were achieved in children under the age of 10 years (BHB = 4.3 mM +/- 0.6 SEM, acetoacetate = 1.8 mM +/- 0.3 SEM) than in 10--18 year olds (BHB = 1.6 mM +/- 0.2 SEM, acetoacetate = 0.57 mM +/- 0.08 SEM). Plasma BHB and acetoacetate levels in children maintained on a 3:1 high fat diet were similar to those in children on a 60% MCT diet. Plasma levels of BHB showed a significant correlation with anticonvulsant effect (P less than 0.02). Both the ketonemia and the anticonvulsant action were reversed rapidly by intravenous infusion of glucose.



Pediatr Neurol. 1985 Mar-Apr;1(2):104-8.

Early biochemical and EEG correlates of the ketogenic diet in children with atypical absence epilepsy.

Ross DL, Swaiman KF, Torres F, Hansen J.

Division of Pediatric Neurology, University of Minnesota Medical School, Minneapolis.

Early changes in blood chemistry and the electroencephalogram were monitored during the first three hours after initiating the medium chain triglyceride (MCT) diet in nine children with intractable atypical absence seizures. Serum glucose, insulin, triglycerides, cholesterol, free fatty acids, ketone bodies concentrations, and venous pH were assayed before and at timed intervals after MCT oil was administered orally. The concentration of serum ketones rose progressively over three hours, beta-hydroxybutyrate proportionately higher than acetoacetate. A statistically significant decrease in the group mean number of epileptiform discharges occurred following MCT therapy. Seizure frequency decreased by more than 50 percent in two-thirds of the children during the 10 week treatment period.

Epilepsy Res. 1999 Dec;37(3):181-90.
Clinical efficacy of the ketogenic diet.

Vining EP.

Pediatric Neurology, Johns Hopkins Hospital, Baltimore, MD 21287-7247, USA.

The ketogenic diet is an effective alternative therapy used to control intractable seizures. It was originally described in 1921 as a way to duplicate and prolong the beneficial effects that fasting appeared to have on seizure control. It involves consuming a calorie-restricted diet in which the fat:carbohydrate + protein ratio ranges from 2:1 to 5:1. Recent prospective studies in children demonstrate that about 50% of children will continue on the diet for at least a year, with 40-50% of those starting the diet having a >50% reduction in seizures after 12 months. When the diet is discontinued it is usually due to lack of efficacy. The diet is a radical medical therapy and nutritional well-being is a constant concern. Renal stones have occurred in 5-8% of children on the diet; lipids are elevated, but the significance of this is not known. The mechanism of action of the diet remains unknown, and it is difficult to assess which biochemical parameters should be monitored as adjustments are made to the diet.


An Esp Pediatr. 1989 Mar;30(3):155-8.

[Evaluation of the effectiveness of the ketogenic diet with medium-chain triglycerides, in the treatment of refractory epilepsy in children. Apropos of a series of cases]


Ros Perez P, Zamarron Cuesta I, Aparicio Meix M, Sastre Gallego A.

Servicio de Pediatria, Hospital Ramon y Cajal, Madrid.

Nine patients with refractory epilepsy were treated with a ketogenic diet. All of them had daily seizures with variable length. These patients, aged between 16 months and 13 years old, showed the following epileptic syndromes: Lennox-Gastaut syndrome's (5 cases); epilepsy with myoclonic absences (1 case); "intermediary petit mal" (1 case); benign atypical partial epilepsy in infancy (1 case), and epilepsy with myoclonic-astatic seizures. For a total of 8 patients (88%) we observed a positive response to both the control of seizures and psychic abilities. In five of these cases (55%) the seizure were controlled totally and was possible to reduce the co-adjuvant drugs. In the other 3 patients (33%) the improvement was just partial. Only for one patient the treatment was interrupted due to secondary effects. The results point out the importance of a right diagnostic, an early treatment with ketogenic diet and familiar training in the improvement of the patients. Finally, we also want to remark that a close relationship with a dietetic and nutritional service is essential in order to get an effective and successful diet.

ediatrics. 1998 Dec;102(6):1358-63.

The efficacy of the ketogenic diet-1998: a prospective evaluation of intervention in 150 children.

Freeman JM, Vining EP, Pillas DJ, Pyzik PL, Casey JC, Kelly LM.

Division of Pediatric Epilepsy, Departments of Neurology and Pediatrics, the Johns Hopkins Medical Institutions, Baltimore Maryland, USA.

OBJECTIVE: The ketogenic diet is a high-fat, low-protein, low-carbohydrate diet developed in the 1920s for the treatment of children with difficult to control seizures. Despite advances in both the pharmacotherapy and the surgery of epilepsy, many children continue to have difficult-to-control seizures. This prospective study sought to determine the ketogenic diet's effectiveness and tolerability in children refractory to today's medications. METHODS: One hundred fifty consecutive children, ages 1 to 16 years, virtually all of whom continued to have more than two seizures per week despite adequate therapy with at least two anticonvulsant medications, were prospectively enrolled in this study, treated with the ketogenic diet, and followed for a minimum of 1 year. Seizure frequency was tabulated from patients' daily seizure calendars and seizure reduction calculated as percentage of baseline frequency. Adverse events and reasons for diet discontinuation were recorded. RESULTS: The children (mean age, 5.3 years), averaged 410 seizures per month before the diet, despite an exposure to a mean of 6.2 antiepileptic medications. Three months after diet initiation, 83% of those starting remained on the diet and 34% had >90% decrease in seizures. At 6 months, 71% still remained on the diet and 32% had a >90% decrease in seizures. At 1 year, 55% remained on the diet and 27% had a >90% decrease in seizure frequency. Most of those discontinuing the diet did so because it was either insufficiently effective or too restrictive. Seven percent stopped because of intercurrent illness. CONCLUSIONS: The ketogenic diet should be considered as alternative therapy for children with difficult-to-control seizures. It is more effective than many of the new anticonvulsant medications and is well tolerated by children and families when it is effective.

The following study is a three to six year follow up, but that may not be long term enough for some people:

Pediatrics. 2001 Oct;108(4):898-905.

The ketogenic diet: a 3- to 6-year follow-up of 150 children enrolled prospectively.

Hemingway C, Freeman JM, Pillas DJ, Pyzik PL.

Johns Hopkins Medical Institutions, Baltimore, Maryland, USA.

OBJECTIVE: To document the long-term outcome of the 83 children with difficult-to-control seizures who were enrolled prospectively in a study of the efficacy of the ketogenic diet and who had remained on the diet for 1 year. METHODS: A total of 150 consecutive children were entered prospectively into a study of the ketogenic diet's efficacy and tolerability. Three to 6 years after diet initiation, all 150 families were sent a survey inquiring about their child's current health status, seizure frequency, and current anticonvulsant medications. They were asked about their experience with the diet and reasons for discontinuation. Several telephone attempts were made to contact those who did not respond to the written questionnaire. Responses were entered in an Access database and analyzed. RESULTS: In 1999, 3 to 6 years after initiating the diet, 107 of 150 families responded to a questionnaire. Thirty-five additional families were interviewed by telephone, 4 were lost to follow-up, and 4 children had died, unrelated to the diet. Of the original 150 patient cohort, 20 (13%) were seizure-free and an additional 21 (14%) had a 90% to 99% decrease in their seizures. Twenty-nine were free of medications, and 28 were on only 1 medication; 15 remained on the diet. There were no known cardiac complications. CONCLUSION: Three to 6 years after initiation, the ketogenic diet had proven to be effective in the control of difficult-to-control seizures in children. The diet often allows decrease or discontinuation of medication. It is more effective than many of the newer anticonvulsants and is well-tolerated when it is effective.

Note the last study which gave the 3-6 year reference. Some people find that a significant amount of time to be on a 'fad' diet.

[/font]

 

[SavedByGrace3]

I lost 30 pounds in 30 days.
I used to drink 3-4 Pepsi a day... now I just do diet coke.
Nothing white! No bread, rice, pototes, milk, sugar, pasta, chips, soda, etc. Check the back of packages for carb content. You would be surprised at how much sugar finds its way into our food.
Be sure to take a full range of vitamins, minerals, etc..
Drop your carbs to less than 20 per day for the first 2 weeks, then go up to 40 - 60 a day.
Eat a lot of fish, which is both good for your diet and contains essential fats. You can eat things like bacon, hamburger, or any other kind of meat and just about as much as you want of it.... but be sensible!
You might think that this diet would make you lose energy and feel bad. Not me. I felt headachie and dizzy the first couple days until "ketosis" kicked in, and then I actually felt much better and had a great deal of energy. I started losing a pound a day or more.... all while eating bacon, hamburger, eggs, steak, etc etc.
Drink a lot of fluid because the fast metabolism of fat also releases the toxins that are stored in the fat. You need the fluid to help keep things cleaned out.
It seems to work better for some people than others. It works on your blood chemistry and how you body creates and burns fat. My wife tried it at the same time I did and was less successful at actually losing weight. She has type 2 diabeties and consulted her doctor before going on this diet(good advice for anyone). They monitor her blood sugar, cloresteral(sp), and blood pressure very closely. Her sugar stablized, her clorestoral(sp) actually lowered (despite the bacon and other fatty foods) and her blood pressure dropped. I do not fully understand how or why... but it does do things for your body.
Walking a couple miles a day also helps shed the blubber faster.
Good luck and be careful!

 

[catalyst]

[font=verdana, arial, helvetica]Ah yes, you may be asking, but does it function as a weight loss regimen? Well, let's see what one or two people may have discovered.

Pediatrics. 1998 Jan;101(1 Pt 1):61-7.

The effects of a high-protein, low-fat, ketogenic diet on adolescents with morbid obesity: body composition, blood chemistries, and sleep abnormalities.

Willi SM, Oexmann MJ, Wright NM, Collop NA, Key LL Jr.

Department of Pediatrics, Medical University of South Carolina, Charleston 29425, USA.

OBJECTIVE. To evaluate the efficacy and metabolic impact of a high-protein, low-carbohydrate, low-fat ketogenic diet (K diet) in the treatment of morbidly obese adolescents with initial weights of >200% of ideal body weight. METHODS. Six adolescents, aged 12 to 15 years, weighing an average of 147.8 kg (range, 120.6-198.6 kg) and having an average body mass index of 50.9 kg/m (39.8-63.0 kg/m), consumed the K diet for 8 weeks. Daily intake consisted of 650 to 725 calories, which was substantively in the form of protein (80-100 g). The diet was very low in carbohydrates (25 g) and fat (25 g). This was followed by 12 weeks of the K diet plus two carbohydrates (30 g) per meal (K+2 diet). MAIN OUTCOME MEASURES. Anthropometric data and blood and urine were collected at enrollment, during week 1, and at 4-week intervals throughout the course of the study. Resting energy expenditure was measured by indirect calorimetry. Body composition was estimated using dual-energy x-ray absorptiometry, bioelectrical impedance analysis, and urinary creatinine excretion at enrollment and on completion of each phase of the diet. Nocturnal polysomnography and multiple sleep latency testing were conducted at baseline and repeated after an average weight loss of 18.7 kg to determine sleep architecture, frequency and duration of apneas, and daytime sleepiness. RESULTS. Subjects lost 15.4 +/- 1.4 kg (mean +/- SEM) during the K diet and an additional 2.3 +/- 2.9 kg during the K+2 diet. Body mass index decreased 5.6 +/- 0.6 kg/m(2) during the K diet and an additional 1.1 +/- 1.1 kg/m(2) during the K+2 diet. Body composition studies indicated that weight was lost equally from all areas of the body and was predominantly fat. Dual-energy x-ray absorptiometry showed a decrease from 51.1% +/- 2.1% body fat to 44.2% +/- 2.9% during the K diet and then to 41.6% +/- 4.5% during the K+2 diet. Lean body mass was not significantly affected. Weight loss was accompanied by a reduction in resting energy expenditure of 5.2 +/- 1.8 kcal/kg of fat-free mass per day. Blood chemistries remained normal throughout the study and included a decrease in serum cholesterol from 162 +/- 12 to 121 +/- 8 mg/dL in the initial 4 weeks of the K diet. An increase in calcium excretion was accompanied by a decrease in total-body bone mineral content. A paucity of rapid eye movement sleep and excessive slow-wave sleep were seen in all subjects at enrollment. Weight loss led to an increase in rapid eye movement sleep (P < .02) and a decrease in slow-wave sleep (P < .01) to near normal levels. CONCLUSIONS. The K diet can be used effectively for rapid weight loss in adolescents with morbid obesity. Loss in lean body mass is blunted, blood chemistries remain normal, and sleep abnormalities significantly decrease with weight loss.

Int J Obes Relat Metab Disord. 1996 Dec;20(12):1067-72. Related Articles, Links

Weight-loss with low or high carbohydrate diet?

Golay A, Eigenheer C, Morel Y, Kujawski P, Lehmann T, de Tonnac N.

Department of Internal Medicine, University Hospital Geneva.

OBJECTIVE: With obesity being recognized as an important cardiovascular risk factor, it is important to determine the optimal hypocaloric diet for decreasing that risk. The goal of this study was to compare the effects of two hypocaloric diets of similar caloric value, but differing in carbohydrate content (25% and 45%). SUBJECTS: Sixty-eight out-patients were followed for 12 w. DESIGN: The patients were assigned to one of two groups that received either a low (25% CHO, n = 31) or a high (45% CHO, n = 37) carbohydrate hypocaloric diet (5.0 MJ/d, 1200 Kcal/d). RESULTS: After 12 w, the mean weight loss was similar and did not differ significantly between the two groups: 10.2 +/- 0.7 kg (25% CHO) and 8.6 +/- 0.8 kg (45% CHO). Furthermore, loss of adipose tissue was similar, 8.1 +/- 0.5 kg (25% CHO) and 7.1 +/- 0.7 kg (45% CHO). Despite a high protein intake (1.4 g/kg/ideal body weight) there was loss of lean body mass: 2.2 +/- 0.4 kg (25% CHO) and 1.4 +/- 0.3 kg (45% CHO). The waist/hip ratio diminished significantly (P < 0.001) and identically in both groups. The fasting blood glucose (even though normal, along with cholesterol and triglyceride concentrations, were significantly decreased after weight loss. The fasting blood insulin which was mildly elevated before weight loss decreased more markedly with the 25% CHO diet compared to the 45% CHO diet (P < 0.003). The glucose/insulin ratio improved significantly (P < 0.05) after weight loss with both diets (0.17 +/- 0.04 mmol/mU (25% CHO) vs 0.10 +/- 0.03 mmol/mU (45% CHO). CONCLUSIONS: Neither diet offered a significant advantage when comparing weight loss or other, metabolic parameters over a 12 w period. However, considering the greater improvement of fasting blood insulin, the glucose/insulin ratio and blood triglyceride, the low carbohydrate diet (25%) could be more favourable in the long-term. The improvement of fasting blood insulin could be explained by the differences in monounsaturated fat composition in the low carbohydrate diet.


J Clin Endocrinol Metab. 2003 Apr;88(4):1617-23.

A randomized trial comparing a very low carbohydrate diet and a calorie-restricted low fat diet on body weight and cardiovascular risk factors in healthy women.

Brehm BJ, Seeley RJ, Daniels SR, D'Alessio DA.

University of Cincinnati and Children's Hospital Medical Center, Cincinnati, Ohio 45221-0038, USA. bonnie.brehm@uc.edu

Untested alternative weight loss diets, such as very low carbohydrate diets, have unsubstantiated efficacy and the potential to adversely affect cardiovascular risk factors. Therefore, we designed a randomized, controlled trial to determine the effects of a very low carbohydrate diet on body composition and cardiovascular risk factors. Subjects were randomized to 6 months of either an ad libitum very low carbohydrate diet or a calorie-restricted diet with 30% of the calories as fat. Anthropometric and metabolic measures were assessed at baseline, 3 months, and 6 months. Fifty-three healthy, obese female volunteers (mean body mass index, 33.6 +/- 0.3 kg/m(2)) were randomized; 42 (79%) completed the trial. Women on both diets reduced calorie consumption by comparable amounts at 3 and 6 months. The very low carbohydrate diet group lost more weight (8.5 +/- 1.0 vs. 3.9 +/- 1.0 kg; P < 0.001) and more body fat (4.8 +/- 0.67 vs. 2.0 +/- 0.75 kg; P < 0.01) than the low fat diet group. Mean levels of blood pressure, lipids, fasting glucose, and insulin were within normal ranges in both groups at baseline. Although all of these parameters improved over the course of the study, there were no differences observed between the two diet groups at 3 or 6 months. beta- Hydroxybutyrate increased significantly in the very low carbohydrate group at 3 months (P = 0.001). Based on these data, a very low carbohydrate diet is more effective than a low fat diet for short-term weight loss and, over 6 months, is not associated with deleterious effects on important cardiovascular risk factors in healthy women.


Int J Obes. 1979;3(3):201-11. Related Articles, Links

Dietetic treatment of obesity with low and high-carbohydrate diets: comparative studies and clinical results.

Rabast U, Schonborn J, Kasper H.

In spite of numerous studies in the literature, it is still questionable as to whether the isocaloric exchange of carbohydrate and fat, in the form of a diet, leads to different degrees of weight loss. In comparative studies, obese patients given a low-carbohydrate (4.14 MJ [1000 kcal]) formula diet (diet Ia) lost 14.0 +/- 1.4 kg and those given an iso-energetic high-carbohydrate diet (diet Ib) 9.8 +/- 0.9 kg. The degree of weight loss was significantly different. Daily weight losses were 362 g and 298 g respectively. Comparative studies of high and low-carbohydrate (7.83 MJ [1900 kcal]) formula diets (diets IIa and b) with a greater number of calories did not show any significant difference. However, there was a greater mean weight loss with the low-carbohydrate diet (351 g/day) compared with that under the high-carbohydrate diet (296 g/day). Evaluation of 117 patients treated with formula diets resulted in a weight loss of over 9 kg in 102 obese patients and over 18 kg in 52 patients. The good response to the low-carbohydrate diet was partly responsible for the successful therapy.

Acta Paediatr Acad Sci Hung. 1979;20(1):99-103. Related Articles, Links

A comparative study of two diets in the treatment of primary exogenous obesity in children.

Pena L, Pena M, Gonzalez J, Claro A.

One hundred four children, six to fourteen years of age, with primary exogenous obesity were randomly distributed in order to be subjected to two different diets, ketogenic (low carbohydrate) and hypocaloric, for eight weeks. Body weight, serum triglycerides, cholesterol, a glucose tolerance test, blood glucose and plasma insulin determination were performed before and after both diets. The results revealed significant differences in body weight and triglyceride concentrations with the two diets although they were more remarkable with the ketogenic diet. There were significant differences in the fasting insulin levels, insulinogenic index, and insulin concentration after a glucose tolerance test in the patients subjected to a ketogenic diet.[/font]

 

[catalyst]

[font=verdana, arial, helvetica] Samaha et al, 2003. A Low-Carbohydrate as Compared with a Low-Fat Diet in Severe Obesity. NEJM 348:2074-2081.[/font]
[font=verdana, arial, helvetica]

Background The effects of a carbohydrate-restricted diet on weight loss and risk factors for atherosclerosis have been incompletely assessed.

Methods We randomly assigned 132 severely obese subjects (including 77 blacks and 23 women) with a mean body-mass index of 43 and a high prevalence of diabetes (39 percent) or the metabolic syndrome (43 percent) to a carbohydrate-restricted (low-carbohydrate) diet or a calorie- and fat-restricted (low-fat) diet.

Results Seventy-nine subjects completed the six-month study. An analysis including all subjects, with the last observation carried forward for those who dropped out, showed that subjects on the low-carbohydrate diet lost more weight than those on the low-fat diet (mean [±SD], –5.8±8.6 kg vs. –1.9±4.2 kg; P=0.002) and had greater decreases in triglyceride levels (mean, –20±43 percent vs. –4±31 percent; P=0.001), irrespective of the use or nonuse of hypoglycemic or lipid-lowering medications. Insulin sensitivity, measured only in subjects without diabetes, also improved more among subjects on the low-carbohydrate diet (6±9 percent vs. –3±8 percent, P=0.01). The amount of weight lost (P<0.001) and assignment to the low-carbohydrate diet (P=0.01) were independent predictors of improvement in triglyceride levels and insulin sensitivity.

Conclusions Severely obese subjects with a high prevalence of diabetes or the metabolic syndrome lost more weight during six months on a carbohydrate-restricted diet than on a calorie- and fat-restricted diet, with a relative improvement in insulin sensitivity and triglyceride levels, even after adjustment for the amount of weight lost. This finding should be interpreted with caution, given the small magnitude of overall and between-group differences in weight loss in these markedly obese subjects and the short duration of the study. Future studies evaluating long-term cardiovascular outcomes are needed before a carbohydrate-restricted diet can be endorsed.


[/font][font=verdana, arial, helvetica] Foster et al, 2003. A Randomized Trial of a Low-Carbohydrate Diet for Obesity. NEJM 348:2082-2090.

[/font][font=verdana, arial, helvetica]Background Despite the popularity of the low-carbohydrate, high-protein, high-fat (Atkins) diet, no randomized, controlled trials have evaluated its efficacy.

Methods We conducted a one-year, multicenter, controlled trial involving 63 obese men and women who were randomly assigned to either a low-carbohydrate, high-protein, high-fat diet or a low-calorie, high-carbohydrate, low-fat (conventional) diet. Professional contact was minimal to replicate the approach used by most dieters.

Results Subjects on the low-carbohydrate diet had lost more weight than subjects on the conventional diet at 3 months (mean [±SD], –6.8±5.0 vs. –2.7±3.7 percent of body weight; P=0.001) and 6 months (–7.0±6.5 vs. –3.2±5.6 percent of body weight, P=0.02), but the difference at 12 months was not significant (–4.4±6.7 vs. –2.5±6.3 percent of body weight, P=0.26). After three months, no significant differences were found between the groups in total or low-density lipoprotein cholesterol concentrations. The increase in high-density lipoprotein cholesterol concentrations and the decrease in triglyceride concentrations were greater among subjects on the low-carbohydrate diet than among those on the conventional diet throughout most of the study. Both diets significantly decreased diastolic blood pressure and the insulin response to an oral glucose load.

Conclusions The low-carbohydrate diet produced a greater weight loss (absolute difference, approximately 4 percent) than did the conventional diet for the first six months, but the differences were not significant at one year. The low-carbohydrate diet was associated with a greater improvement in some risk factors for coronary heart disease. Adherence was poor and attrition was high in both groups. Longer and larger studies are required to determine the long-term safety and efficacy of low-carbohydrate, high-protein, high-fat diets.[/font]

 

[catalyst]

[font=verdana, arial, helvetica]Effects on the metabolism of tumors:

J Am Coll Nutr. 1995 Apr;14(2):202-8. Related Articles, Links

Effects of a ketogenic diet on tumor metabolism and nutritional status in pediatric oncology patients: two case reports.

Nebeling LC, Miraldi F, Shurin SB, Lerner E.

Nutrition Department, Case Western Reserve University, School of Medicine, Cleveland, Ohio, USA.

OBJECTIVE: Establish dietary-induced ketosis in pediatric oncology patients to determine if a ketogenic state would decrease glucose availability to certain tumors, thereby potentially impairing tumor metabolism without adversely affecting the patient's overall nutritional status. DESIGN: Case report. SETTING: University Hospitals of Cleveland. SUBJECTS: Two female pediatric patients with advanced stage malignant Astrocytoma tumors. INTERVENTIONS: Patients were followed as outpatients for 8 weeks. Ketosis was maintained by consuming a 60% medium chain triglyceride oil-based diet. MAIN OUTCOME MEASURES: Tumor glucose metabolism was assessed by Positron Emission Tomography (PET), comparing [Fluorine-18] 2-deoxy-2-fluoro-D-glucose (FDG) uptake at the tumor site before and following the trial period. RESULTS: Within 7 days of initiating the ketogenic diet, blood glucose levels declined to low-normal levels and blood ketones were elevated twenty to thirty fold. Results of PET scans indicated a 21.8% average decrease in glucose uptake at the tumor site in both subjects. One patient exhibited significant clinical improvements in mood and new skill development during the study. She continued the ketogenic diet for an additional twelve months, remaining free of disease progression. CONCLUSION: While this diet does not replace conventional antineoplastic treatments, these preliminary results suggest a potential for clinical application which merits further research.



J Am Diet Assoc. 1995 Jun;95(6):693-7. Related Articles, Links

Implementing a ketogenic diet based on medium-chain triglyceride oil in pediatric patients with cancer.

Nebeling LC, Lerner E.

Nutrition Department, Case Western Reserve University, Cleveland, Ohio 44106-4906, USA.

Traditionally, a ketogenic diet is given to drug-resistant children with epilepsy to improve seizure control. Inducing a ketogenic state in patients with cancer may be a useful adjunct to cancer treatment by affecting tumor glucose metabolism and growth while maintaining the patient's nutritional status. A ketogenic diet consisting of 60% medium-chain triglyceride (MCT) oil, 20% protein, 10% carbohydrate, and 10% other dietary fats was provided to a select group of pediatric patients with advanced-stage cancer to test the effects of dietary-induced ketosis on tumor glucose metabolism. Issues of tolerance and compliance for patients consuming an oral diet (consisting of normal table foods and daily MCT oil "shakes") and for patients receiving an enteral formula are reviewed. Preliminary use of the MCT oil-based diet suggests a potential in pediatric patients with cancer.



Br J Cancer. 1989 May;59(5):677-81. Related Articles, Links

Effect of insulin on weight loss and tumour growth in a cachexia model.

Beck SA, Tisdale MJ.

Pharmaceutical Sciences Institute, Aston University, Birmingham, UK.

A comparison has been made between the effects of daily insulin injection and a ketogenic diet on weight loss and tumour weight in an experimental model of cancer cachexia (MAC16). Weight loss associated with the MAC16 tumour was significantly reduced both by a ketogenic diet (80% MCT) and by daily insulin injections without an increase in either food or water consumption. Animals fed the 80% MCT diet had a significantly reduced tumour weight compared with controls fed a normal laboratory diet, while in animals administered 20 U insulin kg-1 day-1 the tumour weight was 50% greater than in saline infused controls. The stimulation of tumour growth by insulin was counteracted by the inclusion of 3-hydroxybutyrate in the drinking water without any alteration in the extent of weight loss. Depletion of both carcass fat and muscle dry weight in animals bearing the MAC16 tumour was reversed in animals administered either insulin or an 80% MCT diet. Animals bearing the MAC16 tumour had a reduced nitrogen balance compared with non-tumour-bearing controls, mainly due to excess urea excretion, and this was reversed towards control values in animals fed an 80% MCT diet, but not in animals administered insulin. These results suggest that a ketogenic diet is more effective than insulin administration in reversing the cachectic process and has the advantage of a concomitant reduction in tumour weight.[/font]

 

[catalyst]

[font=verdana, arial, helvetica]Metabolism. 1983 Aug;32(8):757-68. Related Articles, Links

The human metabolic response to chronic ketosis without caloric restriction: physical and biochemical adaptation.

Phinney SD, Bistrian BR, Wolfe RR, Blackburn GL.

To study the metabolic effects of ketosis without weight loss, nine lean men were fed a eucaloric balanced diet (EBD) for one week providing 35-50 kcal/kg/d, 1.75 g of protein per kilogram per day and the remaining kilocalories as two-thirds carbohydrate (CHO) and one-third fat. This was followed by four weeks of a eucaloric ketogenic diet (EKD)--isocaloric and isonitrogenous with the EBD but providing less than 20 g CHO daily. Both diets were appropriately supplemented with minerals and vitamins. Weight and whole-body potassium estimated by potassium-40 counting (40K) did not vary significantly during the five-week study. Nitrogen balance (N-Bal) was regained after one week of the EKD. The fasting blood glucose remained lower during the EKD than during the control diet (4.4 mmol/L at EBD, 4.1 mmol/L at EKD-4, P less than 0.01). The fasting whole-body glucose oxidation rate determined by a 13C-glucose primed constant infusion technique fell from 0.71 mg/kg/min during the control diet to 0.50 mg/kg/min (P less than 0.01) during the fourth week of the EKD. The mean serum cholesterol level rose (from 159 to 208 mg/dL) during the EKD, while triglycerides fell from 107 to 79 mg/dL. No disturbance of hepatic or renal function was noted at EKD-4. These findings indicate that the ketotic state induced by the EKD was well tolerated in lean subjects; nitrogen balance was regained after brief adaptation, serum lipids were not pathologically elevated, and blood glucose oxidation at rest was measurably reduced while the subjects remained euglycemic.[/font]

 

[Oblivious]

Exercise and eating less calories is the only way to lost weight permanently aside from unhealthy ways...

I agree! About 7 years ago I gained 20 lbs, which isn't a bunch but was enough for me to get with it. I don't have a perfect diet, but I eat sensibly, and never overeat. I exercise at least 4 times a week. (and I should be doing more than that! ) I have lost all that weight and have kept it off for 7 years with no problems.

 

[Mistyfogg]

I think fad diets are not good for you in the long run. People eventually go back to their normal ways. The best thing to do is to make life changes about what you eat. Cut back on calories, junk food, high fat, high sugar, drink more water, etc. It just takes common sense. Will power is the thing that needs to be worked on for a true, effective diet.

 

[catalyst]

Why is a ketogenic diet a fad diet?

 

[Jacey]

Why is a ketogenic diet a fad diet?

It's not, is it............or am I missing something??

*goes and gets second cup of coffee*

 

[JOE8585]

boy i have a few things to say to a few different post.

Catalyst,

while it is obvious that you are somewhat knowledgible, and definitly obvious that you know how to cut and paste other peoples articles.

but bottom line is this. Calorie reduction is the only and best way to lose weight. yes you can prove that on the Adkins diet you will lose weight, but what i want you to see is the on this diet you are also restricting calories.

any diet that says not to eat fruits and veggies is pure stupidity. there are more antibiotics, more health improving substance, more vitamins in fruits and veggies than in any other type of food.

you have posted what seems to be a million articles full of diet jargin, that most people will never even understand so as far as i can see you are basically wasting space on this thread. you need all the big words to realize what common sense will make the most clear. cut back on calories, excercise, drink plenty of water, and God forbid do NOT stop eating the most health foods (fruits, veggies)

you posted on this thread studys that show that you lose six times more weight faster on the Adkins diet. and my response to this is, just because you lose faster does not in any way, shape or form mean that you are healthier. if i get desperate i can go out and get HIV or cancer and i will lose weight even faster than on Adkins. just because you lose fast doesn't mean your body is internally heathier.

Didaskalos:

sorry to burst your bubble, but it is impossible to 30 lbs in 30 days.

not to say that the scales didn't say that but, you can't lose that much fat in that amount of time. you either lost a large amount of water and some fat, or you lost some fat and a large amount of lean body mass, or you lost some fat, water and body mass.

which neither of the later two are good things. you goal should not be to simply lose weight. it should be to lose fat and maintain if not gain lean body mass. remember the more lean body mass you have the more calories you will burn.

 

[Dagna]

Joe, just to let you know, Atkins doesn't really restrict fruit and veggies intake. For the first two weeks, no fruit but you need to have 3 cups of veggies. Mostly salad, broccoli, cauliflower, brussel sprouts etc. After the 2 week induction phase, you are encouraged to up your intake of veggies and even add a few fruits, namely berries and some melons, bt of course, you can ultimately have anything so long as you keep in your range of carbs. Atkins mostly focuses on fresh made foods. Nothing processed, no starchy veggies (you can actually have these in small amounts during the maintenence phase). I've probably eaten healthier on the Atkins diet than I have before, mostly because I'm now forced to cook. No more fast food, frozen dinners or just plain not eating.
And yes, you do restrict your calories to some degree. Any diet you do that really. But for some reason, Atkins works better for some people than a traditional diet. Don't know why personally, but if it works and people are healthier, then I see no reason to stop those people from doing it.