Prevention Of Obesity Using Low Carbohydrate Ketogenic Diet
March 2009KUWAIT MEDICAL JOURNAL3Review ArticlePrevention of Obesity Using LowCarbohydrate Ketogenic DietHussein M Dashti1,2, Thazhumpal C Mathew2,3Departments of Surgery and Anatomy, Faculty of Medicine3Department of MLS, Faculty of Allied Health Science, Kuwait University, Kuwait1,2Kuwait Medical Journal 2009, 41 (1) 3 -12ABSTRACTThis review focuses on the effect of low carbohydrateketogenic diet on obese subjects presenting withvarious metabolic syndromes. Here, we providedata from our laboratory and from various otherinvestigators on the therapeutic effectiveness ofketogenic diet on obese subjects. In this review weprovide the rationale behind using ketogenic dietas a treatment of obesity and its beneficial role inneurodegenerative / neurological disorders, diabetes,hyperlipidemia, coronary diseases, cancer etc.Administering ketogenic diet for a relatively longerperiod did not produce any significant side effect.Therefore, based on the data presented in this review,it is recommended that it is safe to use ketogenic dietfor a longer period of time for obesity and associateddisorders.KEY WORDS: coronary diseases, diabetes, hyperlipidemia, ketogenic diet, obesityINTRODUCTIONAlthough, historically obesity has beenconsidered as a sign of a prosperous and wealthysociety, today obesity has become a major healthproblem in both developed and developingcountries. Obesity has been described as a diseaseentity since 1700s. Currently obesity levels areincreasing at a remarkable level all over the world.Data from a recent survey by the US Center forDisease Control indicates that 66% of the USpopulation are overweight, with 32.3% having abody mass index (BMI) of more than 30 kg/m2[1].It is estimated that about 300,000 people die eachyear from obesity related diseases[1]. A similartrend is observed in Kuwait and other Middle Eastcountries[2].CLASSIFICATION OF OBESITYObesity has been defined by body mass index(kg/m2) and waist circumference. According tothe current classification of the World HealthOrganization (WHO), body mass index (BMI)greater than 25 is considered overweight[3]. Anadult who has a BMI of 30 or higher is consideredobese. Obesity is further classified into Class I(BMI 30), Class II (BMI 35) and Class III (BMI 40) obesity. In addition to BMI, increased risk ofobesity associated metabolic disorders is foundin men with waist circumferences greater than orequal to 102 cm and in women with 88 cm[1]. Thisclassification of obesity is primarily based on aWestern population perspective[4]. Therefore, itis necessary to redefine obesity from an Asian orMiddle Eastern viewpoint. In Asians, overweighthas been suggested to start at BMI 23 and also lowerwaist circumference cut-offs for men and womenhave been recommended[4].HEALTH CONSEQUENCES OF OBESITYProblems related to obesity affects almostevery aspect of life[5-6]. The rise in obesity andits complications is a threat to global healthcaresystem. The obesity epidemic of the world is out ofcontrol and none of the current measures show anyimprovement in reversing this global crisis. Earlymeasures to curb obesity and public awareness onAddresss correspondence to:Prof. Hussein M. Dashti, Department of Surgery, Faculty of Medicine, PO Box 24923, 13110, Safat, Kuwait. Tel: (965)25319475, Fax:(965)25333098, E-Mail: tcmkwt@gmail.com
Prevention of Obesity Using Low Carbohydrate Ketogenic Diet4Table 1: Obesity associated risksMild riskModerate risk Low back pain Impaired fertility Increasedrisk duringanesthesia fetal defects dueto maternalobesity Cancer Coronary heartdisease Hyperuricaemia Gout Osteoarthritis Complicationsof pregnancySevere risk Diabetes Dyslipidaemia Hypertension Gall bladderdisease Sleep apnoea Breathlessnessobesity associated diseases are the only way towardsachieving a sustainable health service. Along withthe appropriate measures taken to prevent obesity,priority should be given to the treatment of obesityrelated diseases. The health consequences of obesitycan be categorized into mild, moderate and severetypes depending on the risk involved (Table 1).CONTRIBUTINGFACTORSTOWARDSOVERWEIGHT AND OBESITYObesity results from the interplay betweengenes and environment. Both genes and behaviormay be needed for a person to become overweight.Other factors that regulate body weight are the dietpreferences and the number of calories consumed.One of the genetic components of obesity is insulinresistance which is the probable common pathwayfor metabolic syndrome. It has been shown thatdiet choices and physical activity are the majorcontributing factors towards overweight andobesity. Caloric intake must be equal to the caloricexpenditure to maintain a healthy body weight.Calorie, the unit of energy is defined as the amountof heat needed to raise the temperature of one gramof water by one degree Celsius at sea level. Byeating roughly the same number of calories that thebody requires, the body weight can be maintainedin a stable condition. Obviously, weight gainoccurs when more calories are taken than the bodyrequires. The extra calories taken in are stored asfat within the body. However, this fact is true onlywhen eating a lot of carbohydrate along with fat.On a diet with controlled amounts of carbohydrate,the body will switch from using glucose to fat forproducing energy. This means that a person onlow carbohydrate ketogenic diet (LCKD) can takein as much calories and still loose weight. In otherwords, a person while consuming 3,000 calorieson LCKD will loose weight whereas taking in thesame calories on a low-fat high carbohydrate dietwill gain weight. So the assumption that the onlyway to lose weight is to strictly control the intakeof calories needs to rewritten based on the type ofdiet. Furthermore, while on LCKD diet the appetiteis usually diminished and a person will eat onlyMarch 2009fewer calories. Hence persons on LCKD will haveto burn more fat for producing energy, which willlead to more weight loss.Another factor that needs to be mentioned isthe outcome of certain diet programs that restrictcalorie intake. In such circumstances where dietswith restricted calories are taken, so as to conserveenergy, the overall metabolism in the body shiftsinto a slow survival mode. But after certain period,when it becomes inevitable for the person on thelow calorie diet to go back to a higher-calorie diet,the body metabolism will still remain in its slowsurvival mode of burning calories slowly. Henceit becomes quite difficult to continue or maintainweight loss in such situations.OBESITY IN RELATION TO DIET PREFERENCESSince obesity is the accumulation of excess ofbody fat, excessive fat intake has been discouraged.Less fat and exercise had become the slogan againstobesity to be fit physically and maintain a healthybody. Well, for generations people have triedthis recipe of low fat diet, yet they still get obese.Therefore, what we blindly believe about highcarbohydrate diet could be completely baseless.Various researchers have pointed out the badeffects of a high carbohydrate diet. It is the rootcause of various chronic diseases. Several studies[718]have shown that a diet with a high glycemic loadis independently associated with accelerated aging,development of cardiovascular diseases, type IIdiabetes and certain forms of cancer[7-9].The glycemic index is a rating system for foodsbased on their ability to raise the level of bloodglucose within two hours of their consumption[19].When foods of higher glycemic index are eaten thereis a rapid release of glucose into the bloodstream.The glycemic index of pure glucose or white breadis arbitrarily scored as 100[20]. Foods with highglycemic index induce a rapid release of insulin[19].Thus eating foods with a high glycemic index lead tohigher levels of circulating insulin. This rapid surgein insulin release can cause a relative hypoglycemicperiod within the postprandial period. Thereactive hypoglycemia thus developed with foodsof lower fat and higher carbohydrate contentstimulates the appetite and thus leads to obesity[21].The hyperinsulinemia developed following theconsumption of foods with high glycemic indexhas been implicated in creating atheroscleroticplaques, that can lead to heart disease[22]. Insulinincreases salt and water retention, a mediatorof high blood pressure and correlates with highlevels of triglycerol and low levels of high densitylipoprotein (HDL) cholesterol. Now it is evidentthat high carbohydrate diets increase fasting
March 2009KUWAIT MEDICAL JOURNAL5Table 2: Recommended and restricted food in ketogenic diet[66]Recommended FoodFully Restricted rawns, Shrimps.LobsterMeat: Kababs,Sausages, MincedPoultry: Chicken, EggsCheese: Full fat cheeseSpinach, Watercress, Eggplant,Parsley, Mulberry, Coriander, Mint,Artichoke, Okra, Cabbage, Mushroom,Avocado, Leek, Carrot, Radish, Celery,Cauliflower, Green pepper, Lettuce,Cucumber, Tomato, 10-15 olives/day,Lemon, Strawberry -6/day, Avocado,Berries-10/dayOlive oil (5tablespoon,added to thesalad), Flax seedoilplasma triglycerol concentrations[23-27] and decreaseHDL cholesterol concentrations[28-30]. These changesare associated with enhanced atherogenesis[31].However, it is found that short-term ketogenic dietsimprove the lipid disorders that are characteristicof atherogenic dyslipidemia[32]. Furthermore, highinsulin levels lead to increased risk of breast cancerand polycystic ovarian syndrome[6,19,33]. In addition,other evidence indicates that consumption of ahigh–glycemic-index diet is associated with ahigher risk of diabetes.Excess sugar in the bloodstream also leads to theproduction of free radicals. Free radicals increasesignificantly one hour after sugar consumptionand more than double after two hours. It has beenproven that disrupting the oxidant-antioxidantstatus of the cell will lead to various diseases of thebody[33]. Furthermore, increased sugar decreases theblood levels of vitamin E, which leads to a decreasein the natural ability of the body to fight againstfree radical damage.Carbohydrates increase levels of triglycerol, totalcholesterol, and low density lipoprotein (LDL) anddecreases HDL cholesterol. High ratio of triglycerolto HDL has a 16-fold greater incidence of coronaryevents than those with the low ratio[10.19,22,32]. Inseveral studies, insulin, insulin-like growth factorsand carbohydrates were identified as risk factorsfor cancer. It is quite reasonable to believe thatsugar contributes to the growth and metastasis ofcancer since cancer cells utilize sugar as their energysource. In other studies it was found that sugar is acausative factor in kidney disease, liver disease andshortened life span. Although there is cumulativescientific evidence to show that high carbohydratediets can cause more harm than previously thought,we are still unwilling to accept this fact.Since the 1980’s calories from fat intake droppedfrom 34 to 8%. However, no change in the trend ofobesity has been noticed. Interestingly, even afterall this; the negative image of fat is still in ourmind. In fact, contrary to the common belief, highfat diet has certain therapeutic values. Since 1921,high fat diet was used as an effective alternativetherapy to control intractable seizures[34]. In someCarbohydratesFlour, Potato, MacaroniSpaghetti, Noodles,Bread, Rice, Sugar,Sweets, Honey, CakesFruits/drinksAll fruit juicesAll soft drinkscases, high fat diet was found to be far better thanmodern anticonvulsants. The common argumentagainst the consumption of high-fat diet is that itcauses obesity. However, recent studies show thatthe high fat diet can cure obesity. Since obesityresults from genetic and environmental influences,an individualized approach probably is thebest solution for tackling the obesity problems.Therefore, a low-carbohydrate diet combined withan exercise program, in our experience, can helpselected patients to safely achieve weight loss andovercome several obesity associated diseases. Asmentioned earlier, since lower insulin levels andless hunger are the physiologic effects of consumingfoods with low–glycemic-index, persons who takein low-carbohydrate diets could successfully losetheir weight. Furthermore, there is an increasedcalorie use via ketogenesis. Therefore, LCKD isa reasonable alternative for body weight loss forpersons who are willing to adhere to this diet. Table2 gives a brief list of recommended and restrictedfood in ketogenic diet.Low carbohydrate ketogenic dietsLCKD is not new to our society. Even early man’sprehistoric diets may have been low carbohydrateketogenic diets[35]. Prior to its use as a diet forobesity, LCKD have been used in the treatment ofdiabetes[36] and pediatric epilepsy[34]. Also, studieson the therapeutic role of LCKD in obesity are notnew at all. Since 1955, scientists were experimentingon the concept that fat can be eaten ad libitum andstill induce weight loss in obese subjects. A highfat diet changes the body’s metabolism to a newdirection. Incomplete oxidation of fatty acids by theliver, results in the accumulation of ketone bodies inthe body. The condition in which ketone bodies areformed in excess of the body’s ability to metabolizethem is called ketosis. Since high-fat diet causesketosis, they are generally called as ketogenic diets.Ketosis has a significant influence on suppressinghunger. Thus, a ketogenic diet is a good regulatorof the body’s calorie intake and it is the body’snatural adaptation to starvation. However, thismild ketosis has been always confused by the
6Prevention of Obesity Using Low Carbohydrate Ketogenic Dietgeneral public with the dangerous ketoacidosiswhich is associated with untreated type 1 diabetes.But these two conditions are quite different andvirtually opposite. Diabetic ketoacidosis has highblood sugar while ketosis has a high blood level ofketone bodies. Is ketosis safe? If ketosis was bad forhealth, why does nature switch on to a situationsimilar to that of administering a ketogenic diet?Well, everyone approaches ketogenesis during thesleep portion of the diurnal cycle. Above all, whocan ignore the fact that mother’s milk, which hasa high fat content, is the best natural food formulataken in during human development? It is alsointeresting to note that no species could havesurvived millions of years, if its members couldnot tolerate occasional brief periods of naturalstarvation, which results in ketosis.WHAT ARE KETONE BODIES?Ketone bodies result from the partial oxidationof free fatty acids and are synthesized only in themitochondria of liver cells. There are three typesof ketone bodies. They are: acetoacetate (AcAc),ß-hydroxybutyrate (BHB), and acetone. Ketonebodies are always being produced under normaldietary conditions but in amounts that are too smallto cause any metabolic effects[37]. Triacylglycerol(TAG) stored in fat tissue breaks down intoglycerol and three fatty acid molecules. Thisprocess is lipolysis and is regulated by hormoneslike glucagon, epinephrine etc. These hormonesactivate the hormone-sensitive lipase (HSL) thathydrolyzes fatty acid from carbon atom 1 and / or3 of TAG. The remaining fatty acids are removed byother lipases that are specific for diacylglycerol ormonoacylglycerol[38].Fatty acids are classified into short-mediumchain fatty acids consisting of 12 carbons or lessand long chain fatty acids. Medium chain fattyacids are found in the maternal milk and inmedium chain fatty acid oils. The free fatty acidsthat diffuse from adipose cells either bind withalbumin in the blood or remain as free fatty acids.The albumin bound fatty acids are transportedto other tissue to be oxidized and the unboundfree fatty acids present in the blood reach theliver[38, 39]. The medium chain fatty acids enter theliver without any transporter whereas the longchain fatty acids, the major precursor for ketonebodies, need a special transporter called carinitineto enter the mitochondrial matrix and becomeoxidized[40].The medium chain fatty acids become activatedto fatty acyl CoA and undergo ß-oxidation to formfatty acetyl CoA whereas the long chain fatty acidsbecome activated into fatty acyl CoA in the liverMarch 2009cytosol. The carinitine acyltransferase systemmoves the acyl CoA to the mitochondrial matrixwhere they undergo ß-oxidation to form acetylCoA[40]. When there is an excess of acetyl CoA, morethan that is required for providing energy throughKerb’s cycle, the liver converts the extra acetyl CoAinto ketone bodies[41,42].The formation of ketone bodies occurs as follows.Two molecules of acetyl CoA are condensed toform a molecule of acetoacetyl CoA. Then a thirdmolecule of acetyl CoA is added to acetoacetyl CoAto form 3-hydroxy-3-methylglutaryl CoA (HMGCoA). Formation of HMG CoA is catalyzed by thehepatic enzyme, HMG CoA synthase. HMG CoAis then cleaved into acetyl CoA and acetoacetateby the action of another enzyme, HMG CoA lyase.Acetoacetate is either reduced to ß-hydroxybutyrate(BHB) through the action of BHB dehydrogenase orundergoes spontaneous decarboxylation to acetonewhich is excreted in the breath and urine[41,42].Ketone bodies are used as an energy source inthe body including the brain. BHB is convertedto acetoacetate by the reversal reaction of BHBdehydrogenase, producing nicotinamide adeninedinucleotide phosphate (NADH). The acetoacetate,in turn, will bind to coenzyme A (CoA) providedfrom succinyl CoA molecules through thiophorasereaction producing acetoacetyl CoA. The acetylCoA is further converted into two molecules ofacetyl CoA, which will enter the Kreb cycle forproduction of energy[42].EFFECT OF KETOGENIC DIET IN PREVENTINGOBESITYRecent studies from our laboratory haveshown that the ketogenic diet is a natural therapyfor obesity even in diabetic subjects. The weightand body mass index of the patients decreasedsignificantly (p 0.0001) from week 1 to 56 (Table3). A similar significant (p 0.0001) weight loss wasobserved in diabetic subjects who were on a LCKDdiet (Table 4).Several possible mechanisms on the role of verylow carbohydrate diet in reducing body weighthave been suggested[43]. It is thought that major partof the weight loss following the administration ofketogenic diet can be attributed to the loss of water.Each 1 g of glycogen is stored in 3 gms of water.This means that the initial weight loss could bedue to glycogen depletion and water excretion inurine. The weight lost in this manner will be gainedimmediately after stopping the ketogenic diet.Glycogen stores replenishes again with retention ofa large amount of water as mentioned above[44,45].Ketones have a diuretic effect and hence lead to aneven greater water loss[44]. Furthermore, there is a
March 2009KUWAIT MEDICAL JOURNALdecrease in metabolic efficiency resulting in greaterloss of energy in the form of heat[46] and in the formof ketones in urine, sweat, and feces.In addition to the weight loss observed,very-low-carbohydrate ketogenic diets alterthe metabolic rate by preserving more leanbody mass[47]. Following the administration ofketogenic diet there is a preferential loss of fatmass and preservation of more lean body mass[4749]. As mentioned earlier, ketone bodies especiallyBHB, has an effect on appetite suppression[50]. Inaddition, the high fat content in LCKD delays thedigestion providing a sense of fullness[51]. Aboveall, the utilization of fat as body fuel, promote fatloss and therefore weight loss[52]. In addition tostudies from our laboratory, several other studieshave shown that low carbohydrate diets comparedto low fat diets have a significant long term effecton the reduction of body weight[53-55].OTHER BENEFICIAL EFFECTS OF KETOGENICDIETAlthough, the main focus of this review is on thebeneficial effects of ketogenic diet on obesity, weknow that this review will not be complete, if someof the other beneficial effects of ketogenic diets arenot mentioned. Therefore, we give here below, somewell known beneficial effects of ketogenic diet onneuronal and cardiac efficiency and its therapeuticrole in diabetes, heart diseases, cancer etc.7works is still unclear? Several mechanisms thatcontribute to the anticonvulsant role of LCKDhave been suggested. It is found that ketogenicdiet increases the synthesis of the inhibitoryneurotransmitter γ-aminobutyric acid (GABA)in the brain, which may be involved in thesuppression of the seizure activity[58]. Furthermore,LCKD increases the level of polyunsaturated fattyacids (PUFAs), which functions as modulatorsof neuronal membrane excitability by inhibitingthe sodium and calcium ion channels[59]. It issuggested that free radicals contribute to thedevelopment and progression of epilepsy. Thus,the anticonvulsant role of ketogenic diet could alsobe through the antioxidant mechanisms activatedby fatty acids and ketones[60]. It has also been foundthat a ketogenic diet affects signal transduction inneurons by inducing changes in the basal statusof protein phosphorylation[61]. Furthermore,ketogenic diet has beneficial influence on the brainenergy metabolism[62].This is quite significant, ascerebral hypometabolism is a characteristic featureof those who suffer from depression or mania[62].Interestingly, it is shown that a ketogenic dietreduces amyloid ß 40 and 42 in a mouse model ofAlzheimer’s disease[63].Brain functionIn humans, ketone bodies are the only additionalbrain energy source after glucose[56,57]. Hepaticgeneration of ketone bodies during fasting is aprotective mechanism that spares the destructionof muscle from glucose synthesis. Historically, itis known that ketogenic diet is quite effective inantiepileptic treatments. However, how this dietCardiovascular DiseasesThe common notion is that a ketogenic diet willcause high cholesterol, TAG, and cardiovasculardisease because of the high fat it contains. In ourprevious studies and recent studies using ketogenicdiet it is shown that LCKD decreased the levelof triglycerol and LDL cholesterol and increasedthe level of HDL cholesterol[53,64-67]. Furthermore,administering a ketogenic diet for a relativelylonger period of time did not show any significantside effects in the patients. A similar situation wasfound when obese subjects with high cholesterolTable 3: Statistical significance between week 1 and week 56observation of various parameters studied in normal subjects[67].Table 4: Statistical significance between week 1 and week 56observation of various parameters studied in diabetic subjects[67].Normal Subjects (n 33)Diabetic Subjects (n 31)Week 1Week 56p-valueWeight (kg)105.273 15.37774.923 11.384 0.0001Weight (kg)Total chol (mmol/l)5.479 1.2934.650 0.4950.0020Total chol (mmol/l) 6.755 1.0864.878 0.533 0.0001HDL (mmol/l)1.237 0.2701.621 0.177 0.0001HDL (mmol/l)1.033 0.2641.586 0.211 0.0001LDL (mmol/l)4.030 1.1482.807 0.496 0.0001LDL (mmol/l)5.160 0.8923.379 0.608 0.0001TG (mmol/l)1.827 0.9810.861 0.1790.0001TG (mmol/l)4.681 2.4681.006 0.205 0.0001Glucose (mmol/l)5.127 0.4404.726 0.5290.0069Glucose (mmol/l)10.481 3.0264.874 0.556 0.0001Urea (µmol/l)5.563 1.2994.419 0.743 0.0001Urea (µmol/l)5.778 0.9054.972 1.050 0.0111HDL high density lipoprotein; LDL low density lipoprotein;TG TriglycerideData is expressed as mean standard deviation.Week 1Week 56108.081 21.245 83.536 18.030p-value 0.0001HDL high density lipoprotein; LDL low density lipoprotein;TG TriglycerideData is expressed as mean standard deviation.
8Prevention of Obesity Using Low Carbohydrate Ketogenic DietMarch 2009Table 5: Baseline values of different physical and biochemical parameters monitored in persons (high cholesterol / normal cholesterol)subjected to low carbohydrate diet (ketogenic diet) [66]TotalGroup I (n 35)(High cholesterol)Group II (n 31)(Normal cholesterol)p-valueAge (years)42.9 10.845.5 9.239.9 11.80.0731Weight (kg)106.9 18.3112.3 19.3100.7 15.30.0168BMI (kg/m2)39.1 6.140.1 6.138.0 6.10.1385Total chol (mmol/l)6.1 1.47.0 0.95.0 0.8 0.0001HDL (mmol/l)1.1 0.31.1 0.31.2 0.30.0076LDL (mmol/l)4.6 1.25.4 0.83.6 0.7 0.0001TG (mmol/l)3.2 2.34.3 2.62.0 1.1 0.0001Glucose (mmol/l)7.7 3.49.4 3.75.7 1.5 0.0001HDL high density lipoprotein; LDL low density lipoprotein; TG TriglycerideData is expressed as mean standard deviationlevel and obese diabetic subjects were treated withLCKD for longer period, suggesting that it is safe touse ketogenic diet in both diabetic subjects (Table3, 4) and in subjects with high cholesterol level(Table 5, 6). Further studies revealed that despitethe increase of cholesterol intake with ketogenicdiet, there is no significant increase in the totalcholesterol or LDL[53,64-67]. This may be due to thelow insulin level which will activate HMG CoAlyase, the enzyme responsible for ketone formationand inhibit HMG CoA reductase, the enzymeresponsible for cholesterol formation[68]. In a recentstudy from our laboratory on experimental rats,we have convincingly shown that LCKD enhancescardiac tolerance to global ischemia as compared torats fed on a high carbohydrate diet [69]. In addition,ultra structural studies have shown that there wasa decrease in the number of mitochondria in ratsfed a high carbohydrate diet and an increase in thenumber of mitochondria in those fed a LCKD ascompared to the normal diet group, confirming thephysiological observations on cardio-protectivefunction of LCKD[69]. It should be noted that prehistoric diets were high in dietary protein and fat.However, these pre-historic societies were relativelyfree of several cardiovascular diseases that existtoday in our society[35].Diabetes mellitus and insulin resistanceIn the pre-insulin era LCKD has been used fordiabetes treatment instead of medications[70]. Theresults from our laboratory show that LCKD hassignificant beneficial effects in obese diabetic subjectsfollowing its long-term administration (Table 3, 4).The blood glucose level decreased significantly fromthe start until the 56th week. A similar situation wasfound when obese subjects with high cholesterollevel were treated with LCKD for a longer period.As previously mentioned, these studies suggest thatit is safe to use ketogenic diet in both obese diabeticsubjects and subjects with high cholesterol level(Table 5, 6). Furthermore, LCKD may be effectivefor improving glycemia and reducing medicationsin patients with type 2 diabetes.Insulin resistance is a characteristic feature ofType 2 diabetes[71]. Insulin resistance is defined as theinability of insulin to produce its usual response atconcentrations that are effective in normal individuals.As mentioned earlier, the content of carbohydrate inthe diet is the most important factor that influencesTable 6: Percentage changes in the various parameters observed at week 56 in persons (high cholesterol / normal cholesterol) subjectedto ketogenic diet[66]Total (n 66)Group I (n 35)High cholesterolGroup II (n 31)Normal cholesterolp-valueWeight (kg)-25.9 6.3-25.8 6.7-26.0 5.80.9065Total chol (mmol/l)-19.3 17.0-29.2 9.4-6.2 16.20.0005HDL (mmol/l)52.3 43.863.7 52.737.1 20.60.1778LDL (mmol/l)-28.2 20.1-33.5 19.5-21.3 19.10.1331TG (mmol/l)-59.0 32.1-69.8 32.6-44.7 25.70.0537Glucose (mmol/l)-31.0 25.0-44.0 22.6-12.8 15.10.0004HDL high density lipoprotein; LDL low density lipoprotein; TG TriglycerideData is expressed as mean standard deviation. Statistical significance between Group I and Group II are given.
March 2009KUWAIT MEDICAL JOURNALTable 7: Statistical significance between week 1 and week 56observation of various parameters studied in group I (highcholesterol) and group II (normal cholesterol) subjects[66].Total(n 66)Group I(n 35) HighcholesterolWeight (kg) 0.0001 0.0001 0.0001BMI (kg/m ) 0.0001 0.0001 0.0001Total chol (mmol/l) 0.0001 0.00010.0170HDL (mmol/l) 0.0001 0.0001 0.0001LDL (mmol/l) 0.0001 0.0001 0.0001TG (mmol/l) 0.0001 0.00010.0002Glucose (mmol/l) 0.0001 0.00010.00342Group II(n 31) Normalcholesterol)BMI Body mass index, Chol cholesterol, HDL high densitylipoprotein; LDL low density lipoprotein; TG Triglyceridethe glycemic level. LCKD appear to improve glycemiccontrol and le ssen the need for exogenous insulinand hypoglycemic medication[67,72]. Furthermore,LCKD significantly improved the insulin sensitivityby up to 75%[54,73]. In a recent study on experimentalrats from our laboratory, we have demonstratedthat LCKD ameliorated the diabetic state andhelped to stabilize hyperglycemia. In addition to itstherapeutic effect, LCKD had a significant protectiverole against the diabetogenic action of streptozotocin(STZ) [74]. STZ is selectively cytotoxic to the ß-cells ofpancreatic islets. Therefore it is commonly used toinduce diabetes in experimental animals[74].OsteoporosisA link between low fat diet and osteoporosis hasbeen suggested. Very-low-fat diets are considered tobe low in calcium content. Women on low-fat dietsexcrete most of the calcium they consume. Therefore,they are more prone to osteoporosis. On the otherhand recent studies indicate that a high fat diet canrectify this situation[75].CancerThe relation between high fat diet and cancer isclose to reality now. It has been found that alteredenergy metabolism and substrate requirements oftumor cells can provide a target for cancer therapy.Two major metabolic alterations found in cancer cellsare the increase in glucose consumption and aerobicglycolysis, the conversion of glucose to lactic acidvia the reduction of pyruvate even in the presence ofoxygen. In addition, there are defects in ketone bodymetabolism[71,76]. These metabolic changes in cancercells may provide a rationale for therapeuticstrategies that inhibit tumor growth by LCKD.It has been shown that cancers, specifically braintumors grow minimally on a LCKD[77]. These studies9suggest that treatment with LCKD is a safe andeffective alternative therapeutic option for malignantbrain cancer. In addition, ketone bodies funct
The glycemic index is a rating system for foods based on their ability to raise the level of blood glucose within two hours of their consumption[19]. When foods of higher glycemic index are eaten there is a rapid release of glucose into the bloodstream. The glycemic index of pure glucose or white bread is
Prevalence of obesity and severe obesity in US children, 1999‐2014. Obesity, 2016 May;24(5):1116-23. Wang et al. What childhood obesity prevention programmes work? A systematic review and meta-analysis. Obes Rev, 2015 Langford et al. Obesity prevention and the Health Promoting Schools framework: essential components and barriers to .
1.1 Childhood obesity 13 1.2 Key global strategies related to obesity prevention 13 1.3 WHO Forum and Technical Meeting on Population-based Prevention Strategies for Childhood Obesity 15 1.4 Purpose and structure of the document 15 Guiding principles for the development of a population-based childhood obesity prevention strategy 16
Obesity Obesity is a disease where a person’s weight is in an unhealthy range (BMI of 30.0-39.9). It is a disease that can lead to other health problems. Talk with your healthcare provider to better understand and treat obesity. Severe Obesity Someone who is more than 100 pounds over their
2. Obesity trends and co-morbid consequences. 3. Poverty, obesity and food econo-mics. 4. Genetics and Caribbean culture. 5. The cost of obesity to develop-ment. Dimensions 1- Obesity Epide-miology: Prevalence, Age and Gender Relationships The most striking features of Figure 1 are (a) the high prevalence of overweight (BMI 25) and obesity
that obesity and extreme obesity rates have declined among low-income preschool children. If the current trends in childhood obesity can be reversed, children will have greater opportunities for healthier lives with better results. This document examines childhood obesity in Pennsylvania and efforts made by stakeholders, such as philanthropists,
Childhood Obesity Childhood obesity has both immediate and long-term effects on health and well-being. The increas-ing number of children who are obese has led federal policymakers to rank childhood obesity as a critical health threat. Multiple approaches are necessary to address the challenge of childhood obesity, and health profes-
Obesity Prevention and Control THE PUBLIC HEALTH CHALLENGE Obesity is common, serious, and costly z About 36% of adults and 17% of children and adolescents are obese.1 z Obesity affects all race/ethnicity groups, with higher rates among African-American and Hispanic children and adults.3, 4 z An estimated 1 in 8 preschool children from low income households is obese.5
of obesity is related to the increase of metabolic syndrome, a cluster of central obesity, insulin resistance, hypertension and dyslipidemia. Metabolic syndrome is a known risk factor for the cardiovascular disease and diabetes in the adolescents and adults. Adolescent obesity is a strong precursor of obesity and related morbidity in adulthood .
