Research studies that formed the basis
for the SlimXpress™Weight Loss &
The SlimXpress™ diet is a high protein/low carbohydrate, ketogenic diet* or ketosis diet. The following research and medical studies formed the basis for our diet and laid the foundation for our SlimXpress™ weight loss and wellness program. We do not make any claim that while on the SlimXpress™ diet you will receive any of the weight loss or health benefits reported in these studies.
These studies are simply listed to show why we chose a high lean protein/low carbohydrate, ketosis diet as a basis for the SlimXpress™ weight loss and wellness program. As more research becomes available on these dietary approaches for weight loss and health improvements they will be listed on our research study page. If you do not agree with the results of these studies please contact the authors of the studies as we only report the results of and not our opinion of the studies.
*Our diet is a modified ketogenic diet in that we replaced the high fat of a typical ketogenic diet with high lean protein.
Faster weight loss (16-17-27) Heart disease (1-4-5) Type 2 diabetes (3-8-9)
CONCLUSION: Short-term high protein weight loss diets had beneficial effects on total cholesterol and triacylglycerol in overweight and obese subjects and achieved greater weight loss and better lipid results in subjects at increased risk of CVD. These observations provide further information regarding the utility of this dietary approach in effectively managing body weight and composition and reducing CVD risk in overweight and obese individuals.
2.) Comparison of the Atkins, Zone, Ornish, and LEARN diets for change in weight and related risk factors among overweight premenopausal women.JAMA. 2007 Mar 7;297(9):969-77. Stanford Prevention Research Center and the Department of Medicine, Stanford University Medical School, Stanford, Calif, USA. firstname.lastname@example.org
CONCLUSIONS: In this study, premenopausal overweight and obese women assigned to follow the Atkins diet, which had the lowest carbohydrate intake, lost more weight at 12 months than women assigned to follow the Zone diet, and had experienced comparable or more favorable metabolic effects than those assigned to the Zone, Ornish, or LEARN diets [corrected] While questions remain about long-term effects and mechanisms, a low-carbohydrate, high-protein, high-fat diet may be considered a feasible alternative recommendation for weight loss.
CONCLUSION: In a small group of obese patients with type 2 diabetes, a low-carbohydrate diet followed for 2 weeks resulted in spontaneous reduction in energy intake to a level appropriate to their height; weight loss that was completely accounted for by reduced caloric intake; much improved 24-hour blood glucose profiles, insulin sensitivity, and hemoglobin A1c; and decreased plasma triglyceride and cholesterol levels. The long-term effects of this diet, however, remain uncertain.
Conclusion: both dietary patterns achieved net weight loss and improvements in cardiovascular risk factors.
5.) Low-carbohydrate diets, obesity, and metabolic risk factors for cardiovascular disease. University of Pennsylvania Medical Center, Philadelphia VA Medical Center, 3900 Woodland Avenue, 8th Floor Cardiology MC 111C, Philadelphia, PA 19104, USA. Rick.email@example.com
Abstract. Given the increased prevalence of obesity in the United States (and its associated cardiovascular risk) despite reduced fat intake, there has been increasing interest in the effect of low-carbohydrate diets on obesity. Recent prospective trials have demonstrated equivalent weight loss on low-carbohydrate versus low-fat diets, but with significantly different effects on metabolic risk factors for cardiovascular disease.
6.) Low-carbohydrate diets have more favorable effects on metabolic abnormalities found in insulin resistance syndromes, including serum triglyceride levels, high-density lipoprotein cholesterol levels, and small, dense low-density lipoprotein particles. PMID: 18377783 [PubMed - indexed for MEDLINE]
Conclusion: The translation of these different metabolic effects on cardiovascular disease and events requires future studies. These studies should take into consideration that patients with insulin resistance syndromes would be the most likely group to benefit from carbohydrate restriction.
7.) The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism.
Abstract. The effects of ketone body metabolism suggests that mild ketosis may offer therapeutic potential in a variety of different common and rare disease states. These inferences follow directly from the metabolic effects of ketosis and the higher inherent energy present in d-beta-hydroxybutyrate relative to pyruvate, the normal mitochondrial fuel produced by glycolysis leading to an increase in the DeltaG' of ATP hydrolysis. The large categories of disease for which ketones may have therapeutic effects are:(1)diseases of substrate insufficiency or insulin resistance,(2)diseases resulting from free radical damage,(3)disease resulting from hypoxia. Current ketogenic diets are all characterized by elevations of free fatty acids, which may lead to metabolic inefficiency by activation of the PPAR system and its associated uncoupling mitochondrial uncoupling proteins. New diets comprised of ketone bodies themselves or their esters may obviate this present difficulty.
8.) A low-carbohydrate, ketogenic diet to treat type 2 diabetes
William S Yancy, Jr, Marjorie Foy, Allison M Chalecki,Mary C Vernon, and Eric C Westman
Conclusion: The low-carbohydrate, ketogenic diet (LCKD) improved glycemic control in patients with type 2 diabetes such that diabetes medications were discontinued or reduced in most participants. Because the LCKD can be very effective at lowering blood glucose, patients on diabetes medication who use this diet should be under close medical supervision or capable of adjusting their medication.
RESULTS: The body weight, body mass index, the level of blood glucose, total cholesterol, LDL-cholesterol, triglycerides, and urea showed a significant decrease from week 1 to week 56 (P < 0.0001), whereas the level of HDL-cholesterol increased significantly (good Cholesterol) (P < 0.0001). CONCLUSION: This study shows the beneficial effects of ketogenic diet in obese diabetic subjects following its long-term administration. Furthermore, it demonstrates that in addition to its therapeutic value, low carbohydrate diet is safe to use for a longer period of time in obese diabetic subjects
10.) A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Center for Health Services Research in Primary Care, Department of Veterans Affairs Medical Center, and Duke University Medical Center, Durham, North Carolina 27705, USA.
Conclusions: Compared with a low-fat diet, a low-carbohydrate diet program had better participant retention and greater weight loss. During active weight loss, serum triglyceride levels decreased more and high-density lipoprotein cholesterol level (HDL) increased more with the low-carbohydrate diet than with the low-fat diet.
11.) Weight and metabolic outcomes after 2 years on alow-carbohydrate versus low-fat diet:a randomized trial.
Conculsion: The effects of a l Successful weight loss can be achieved with either a low-fat or low-carbohydrate diet when coupled with behavioral treatment. A low-carbohydrate diet is associated with favorable changes in cardiovascular disease risk factors at 2 years.
12.) Medical aspects of ketone body metabolism. Mitchell GA, Kassovska-Bratinova S, Boukaftane Y, Robert MF, Wang SP, Ashmarina L, Lambert M, Lapierre P, Potier E.
Ketone bodies are produced in the liver, mainly from the oxidation of fatty acids, and are exported to peripheral tissues for use as an energy source. They are particularly important for the brain, which has no other substantial non-glucose-derived energy source. The 2 main ketone bodies are 3-hydroxybutyrate (3HB) and acetoacetate (AcAc). Biochemically, abnormalities of ketone body metabolism can present in 3 fashions: ketosis, hypoketotic hypoglycemia, and abnormalities of the 3HB/AcAc ratio. Normally, the presence of ketosis implies 2 things: that lipid energy metabolism has been activated and that the entire pathway of lipid degradation is intact. In rare patients, ketosis reflects an inability to utilize ketone bodies.
Ketosis is normal during fasting, after prolonged exercise, and when a high-fat diet is consumed. During the neonatal period, infancy and pregnancy, times at which lipid energy metabolism is particularly active, ketosis develops readily. Pathologic causes of ketosis include diabetes, ketotic hypoglycemia of childhood, corticosteroid or growth hormone deficiency, intoxication with alcohol or salicylates, and several inborn errors of metabolism. The absence of ketosis in a patient with hypoglycemia is abnormal and suggests the diagnosis of either hyperinsulinism or an inborn error of fat energy metabolism. An abnormal elevation of the 3HB/AcAc ratio usually implies a non-oxidized state of the hepatocyte mitochondrial matrix resulting from hypoxia-ischemia or other causes. We summarize the differential diagnosis of abnormalities of ketone body metabolism, as well as pertinent recent advances in research.
13.) A randomized trial of a hypocaloric high-protein diet, with and without exercise, on weight loss, fitness, and markers of the Metabolic Syndrome in overweight and obese women. Appl Physiol Nutr Metab. 2007 Aug;32(4):743-52
Conclusion: A high-protein diet was superior to a low-fat, high-carbohydrate diet either alone or when combined with an aerobic/resistance-training program in promoting weight loss and nitrogen balance, while similarly improving body composition and risk factors for the Metabolic Syndrome in overweight and obese Canadian women.
14.) Ketogenic Diets: An Update for Child Neurologists Eric H. Kossoff, MD, Beth A. Zupec-Kania, RD, and Jong M. Rho, MD
Conclusions: The ketogenic diet remains one of the most effective, yet underused treatments for intractable childhood epi-lepsy. By 2009, the ketogenic diet has become a well-established treatment supported by 2 randomized controlled studies demonstrating efficacy and a recently published international consensus guideline on its use. At no other time in the history of the ketogenic diet have basic and clinical scientists collaborated more to eluci-date its mechanisms of action to ultimately enhance ther-apeutic strategies and to identify appropriate candidates. Given the advances in the field of ketogenic diet research, child neurologists should be reassured in their efforts to use the ketogenic diet and to consider adopting this treatment strategy sooner in the course of epilepsy treatment. 14.b.) KETOGENIC DIETS: NOT JUST FOR EPILEPSY ANY LONGER HTTP://WWW.EPILEPSY.COM/EPILEPSY/KETO_NEWS_AUG08R.
16.) Ketone bodies, potential therapeutic uses. Veech RL, Chance B, Kashiwaya Y, Lardy HA, Cahill GF Jr. IUBMB Life. 2001; 51 :241-7.
17.) Ketosis. Encyclopedia of Human Nutrition, 91-98. Williamson, D.H. (2005).
18.) Induced severe hyperglycaemia and ketoacidosis in a non-diabetic renal transplant recipient. Clin Exp Nephrol. 2009 Feb;13(1):89-91. Epub 2008 Jul
17. Khaira A, Gupta A, Tandon N, Agarwal SK. Gatifloxacin
19.) Life-threatening hyperglycemia and acidosis related to olanzapine: a case report and review of the literature. J Intensive Care Med. 2007 Jan-Feb;22(1):52-5. Varma MK, Connolly K, Fulton B.
21.) Alcoholic ketoacidosis. Adams SL. Emerg Med Clin North Am. 1990 Nov;8(4):749-60.
22.) Diabetic ketoacidosis and hyperglycemic hyperosmolar nonketotic syndrome. Delaney MF, Zisman A, Kettyle WM. Endocrinol Metab Clin North Am. 2000 Dec;29(4):683-705, V.
23.) A case of lactation "bovine" ketoacidosis. J Emerg Heffner AC, Johnson DP. Med. 2008 Nov;35(4):385-7. Epub 2007 Sep 17.
24.) Nondiabetic ketoacidosis caused by severe hyperthyroidism. Wood ET, Kinlaw WB. Thyroid. 2004 Aug;14(8):628-30.
25.) Low-carbohydrate nutrition and metabolism1,2,3
Eric C Westman, Richard D Feinman, John C Mavropoulos, Mary C Vernon, Jeff S Volek, James A Wortman, William S Yancy and Stephen D Phinney
26.) Ketoacidosis Associated with Severe Hypoglycemia Baena MG, Cayón M, Ortego-Rojo J, Aguilar-Diosdado M. Diabetic.J Endocrinol Invest. 2010 Apr 12. [Epub ahead of print]
27.) Fasanmade OA, Odeniyi IA, Ogbera AO. Diabetic ketoacidosis: diagnosis and management. Afr J Med Med Sci. 2008 Jun;37(2):99-105.
28.) Yared Z, Chiasson JL. Ketoacidosis and the hyperosmolar hyperglycemic state in adult diabetic patients. Diagnosis and treatment. Minerva Med. 2003 Dec;94(6):409-18.
29.) Efficacy and Safety of a High Protein, Low Carbohydrate Diet for Weight Loss in Severely Obese Adolescents. Krebs NF, et al. J Pediatr 2010;157:252-8.
30.) Effects of a high-protein ketogenic diet on hunger, appetite, and weight loss in obese men feeding ad libitum. Johnstone AM, Horgan GW, Murison SD, Bremner DM, Lobley GE. American Journal of Clinical Nutrition, Vol. 87, No. 1, 44-55, January 2008.
31.) A low-carbohydrate, ketogenic diet versus a low-fat diet to treat obesity and hyperlipidemia: a randomized, controlled trial. Yancy WS Jr, Olsen MK, Guyton JR, Bakst RP, Westman EC. Ann Intern Med. 2004 May 18;140(10):769-77.
33.) Kodde IF, van der Stok J, Smolenski RT, de Jong JW. Metabolic and genetic regulation of cardiac energy substrate preference. Comp Biochem Physiol A Mol Integr Physiol. 2007 Jan;146(1):26-39. Epub 2006 Oct 3.
34.) Smith SL, Heal DJ, Martin KF.KTX 0101: a potential metabolic approach to cytoprotection in major surgery and neurological disorders. CNS Drug Rev. 2005 Summer;11(2):113-40
35.) Cahill GF Jr, Veech RL. Ketoacids? Good medicine? Trans Am Clin Climatol Assoc. 2003;114:149-61; discussion 162-3.
36.) Suzuki M, Suzuki M, Sato K, Dohi S, Sato T, Matsuura A, Hiraide A. Effect of beta-hydroxybutyrate, a cerebral function improving agent, on cerebral hypoxia, anoxia and ischemia in mice and rats. Jpn J Pharmacol. 2001 Oct;87(2):143-50
37.) Kashiwaya Y, Takeshima T, Mori N, Nakashima K, Clarke K, Veech RL.D-beta-hydroxybutyrate protects neurons in models of Alzheimer's and Parkinson's disease. Proc Natl Acad Sci U S A. 2000 May 9;97(10):5440-4.
38.) Maintenance on a ketogenic diet: voluntary exercise, adiposity and neuroendocrine effects. Kinzig KP, Taylor RJ. nt J Obes (Lond). 2009 Aug;33(8):824-30. Epub 2009 Jun 9
39.) Benefits of ketogenic diets. American Journal of Clinical Nutrition Krilanovich N., Vol. 85, No. 1, 238-239, January 2007.
40.) Wadden TA, Stunkard AJ, Brownell KD, Day SC. A comparison of two very-low-calorie diets: protein-sparing-modified fast versus protein-formula-liquid diet. Am J Clin Nutr. 1985 Mar;41(3):533-9.
41.) Very low-carbohydrate and low-fat diets affect fasting lipids and postprandial lipemia differently in overweight men. Sharman MJ, Gómez AL, Kraemer WJ, Volek JS. J Nutr. 2004 Apr;134(4):880-5.
42.) The effect of ketone bodies on nitrogen metabolism in skeletal muscle. Thompson JR, Wu G. Comp Biochem Physiol B. 1991;100(2):209-16.
43.) Protein sparing during treatment of obesity: ketogenic versus nonketogenic very low calorie diet. Vazquez JA, Adibi SA. Metabolism. 1992 Apr;41(4):406-14.
44). The effects of a high-protein, low-fat, ketogenic diet on adolescents with morbid obesity: body composition, blood chemistries, and sleep abnormalities. William SM, Oexmann MJ, Wright NM, Collop NA, Key LL Jr. Pediatrics. 1998 Jan;101(1 Pt 1):61-7.
45.) A ketogenic diet favorably affects serum biomarkers for cardiovascular disease in normal-weight men. Sharman MJ, Kraemer WJ, Love DM, Avery NG, Gómez AL, Scheett TP, Volek JS. J Nutr. 2002 Jul;132(7):1879-85
46.) Badman MK, Kennedy AR, Adams AC, Pissios P, Maratos-Flier E. A Very Low Carbohydrate Ketogenic Diet Improves Glucose Tolerance in ob/ob Mice Independent of Weight Loss. Am J Physiol Endocrinol Metab. 2009 Sep 8.
47.) Low-carbohydrate diet disrupts the association between insulin resistance and weight gain. Leite JO, DeOgburn R, Ratliff JC, Su R, Volek JS, McGrane MM, Dardik A, Fernandez ML. Metabolism. 2009 Aug;58(8):1116-22. Epub 2009 Jun 18.
48.) The effect of a plant-based low-carbohydrate ("Eco-Atkins") diet on body weight and blood lipid concentrations in hyperlipidemic subjects. Jenkins DJ, Wong JM, Kendall CW, Esfahani A, Ng VW, Leong TC, Faulkner DA, Vidgen E, Greaves KA, Paul G, Singer W. Arch Intern Med. 2009 Jun 8;169(11):1046-54.
49.) Low-carbohydrate diets: nutritional and physiological aspects. Adam-Perrot A, Clifton P, Brouns FObes Rev. 2006 Feb;7(1):49-58.
50.) Effect of a low-carbohydrate, ketogenic diet program compared to a low-fat diet on fasting lipoprotein subclasses. Westman EC, Yancy WS Jr, Olsen MK, Dudley T, Guyton JR. Int J Cardiol. 2006 Jun 16;110(2):212-6. Epub 2005 Nov 16.
51.) Role of glucose and ketone bodies in the metabolic control of experimental brain cancer. Seyfried TN, Sanderson TM, El-Abbadi MM, McGowan R, Mukherjee P.: Br J Cancer. 2003 Oct 6;89(7):1375-82.
52.) Neuroprotective and disease-modifying effects of the ketogenic diet. Gasior M, Rogawski MA, Hartman AL. Behav Pharmacol. 2006 Sep;17(5-6):431-9.
53.) The neuroprotective properties of calorie restriction, the ketogenic diet, and ketone bodies. Maalouf M, Rho JM, Mattson MP. Brain Res Rev. 2009 Mar;59(2):293-315. Epub 2008 Sep 25.
54.) Garai J, Lóránd T, Molnár V. Ketone bodies affect the enzymatic activity of macrophage migration inhibitory factor. Life Sci. 2005 Aug 5;77(12):1375-80.
55.) Targeting energy metabolism in brain cancer with calorically restricted ketogenic diets. Seyfried TN, Kiebish M, Mukherjee P, Marsh J. Epilepsia. 2008 Nov;49 Suppl 8:114-6.
56.) Metabolic control analysis of ketone and insulin action: Implications for phenotyping of disease and design of therapy. Lecture: The Dynamic and Energetic Basis of Health and Aging Veech RL:Nov 13, 2002, The Cloister's, NIH, Bethesda MD.
57.) Masuda R, Monahan JW, Kashiwaya Y: D-beta-hydroxybutyrate is neuroprotective against hypoxia in serum-free hippocampal primary cultures. J Neurosci Res 2005, 80:501-509.
58.) Bough KJ, Rho JM. Anticonvulsant mechanisms of the ketogenic diet. Epilepsia. 2007 Jan;48(1):43-58.
59.) Yancy WS Jr, Westman EC, McDuffie JR, Grambow SC, Jeffreys AS, Bolton J, Chalecki A, Oddone EZ. A randomized trial of a low-carbohydrate diet vs orlistat plus a low-fat diet for weight loss.Arch Intern Med. 2010 Jan 25;170(2):136-45.
60.) Pérez-Guisado J, Muñoz-Serrano A, Alonso-Moraga A. Spanish Ketogenic Mediterranean Diet: a healthy cardiovascular diet for weight loss. Nutr J. 2008 Oct 26;7:30.
61.) Maalouf M, Rho JM, Mattson MP. The neuroprotective properties of calorie restriction, the ketogenic diet, and ketone bodies. Brain Res Rev. 2009 Mar;59(2):293-315. Epub 2008 Sep 25.
62.) Studzinski CM, MacKay WA, Beckett TL, Henderson ST, Murphy MP, Sullivan PG, Burnham WM. Induction of ketosis may improve mitochondrial function and decrease steady-state amyloid-beta precursor protein (APP) levels in the aged dog.Brain Res. 2008 Aug 21;1226:209-17. Epub 2008 Jun 11.
63.) Ketone bodies as a therapeutic for Alzheimer's disease. Henderson ST. Neurotherapeutics. 2008 Jul;5(3):470-80.
64.) Davis LM, Pauly JR, Readnower RD, Rho JM, Sullivan PG. Fasting is neuroprotective following traumatic brain injury.J Neurosci Res. 2008 Jun;86(8):1812-22.
65.) The ketogenic diet increases mitochondrial glutathione levels. Jarrett SG, Milder JB, Liang LP, Patel M. J Neurochem. 2008 Aug;106(3):1044-51. Epub 2008 May 5.
67.) Carbohydrate-restricted diets high in either monounsaturated fat or protein are equally effective at promoting fat loss and improving blood lipids. Luscombe-Marsh ND, Noakes M, Wittert GA, Keogh JB, Foster P, Clifton PM. Am J Clin Nutr. 2005 Apr;81(4):762-72.
68.) The ketogenic diet: uses in epilepsy and other neurologic illnesses. Current Treatment Options in Neurology, vol. 10, no. 6, pp. 410–419, 2008.
69.) Successful Treatment of Type 1 Diabetes and Seizures With Combined Ketogenic Diet and Insulin. Aguirre Castaneda RL, Mack KJ, Lteif A. Jan 2012
70.) The therapeutic implications of ketone bodies: the effects of ketone bodies in pathological conditions: ketosis, ketogenic diet, redox states, insulin resistance, and mitochondrial metabolism. Veech RL: Prostaglandins Leukot Essent Fatty Acids 2004, 70:309-319.
71.) Ketosis and the ketogenic diet, 2010: advances in treating epilepsy and other disorders. Johns Hopkins Medical Institutions, Baltimore, MD, USA. firstname.lastname@example.org
72.) Targeting energy metabolism in brain cancer through calorie restriction and the ketogenic diet
Thomas N Seyfried, Michael Kiebish, Jeremy Marsh, Purna Mukherjee Department of Biology, Boston College, Chestnut Hill, MA 02467, USA
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These statements have not been evaluated by the Food and Drug Administration. These products diets and or procedures are not intended to diagnose, treat, cure, or prevent any disease. No information on this website is intended as personal medical advice and should not take the place of a doctor's care. Please consult your health care provider for advice about a specific medical condition.
We do not make any claim that while on the SlimXpress diet and weight loss and wellness program you will receive any of the weight loss or health benefits reported in these studies.
For more information on the SlimXpress Diet
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