low carb diets significantly increase your risk for insulin resistance and diabetes

WHAT CAUSES INSULIN RESISTANCE?

The overaccumulation of saturated fatty acids from animal products like meat, fish and dairy proucts can saturate the storage capacity of adipose tissue, resulting in a lipid spill over into the liver, muscle, heart, and insulin producting cells in the pancreas. The storage of lipid in tissues that are not designed to store lipid blocks the ability of insulin to do it’s job effectively.

High fat diets are a risk factor for insulin resistanceSaturated fatty acids are the worst offenders

Low Carb Diets are High Fat DietsHigh Fat Diets Reduce Insulin Action

When excess fat accumulates it the muscle and liver tissue, the ability of glucose to enter both tissues is significantly compromised. This is important because blocking glucose from entering the muscle and liver result in high blood sugar. Clear the liver and muscle of fat and

insulin requirements are significantly reduced.

Insulin resistance is caused by lipid overloaddue to a low carb (or high fat) diet

Insulin resistance is the root cause of all forms of diabetes

low fat diets are the gold standard for reversing insulin resistance and type 2 diabetes

Evidence-based research clearly shows that low fatdiets reverse insulin resistance very effectively*

*Please consult the references for more information on these studies

WHAT REVERSES INSULIN RESISTANCE?

Effective at ReducingInsulin Resistance

High Carbohydrate DietHigh carbohydrate intake (>60%)Low fat intake (<15%)Low protein intake (<15%)

15%

15%

70%

Risk Factor forInsulin Resistance

Low Carbohydrate DietLow carbohydrate intake (<40%)High fat intake (>40%)High protein intake (>40%)

40%

50%

10%

FP

C

FP

C

Why is Insulin Resistance Dangerous? Thereisconsiderableevidencetosuggestthatelevationsinfreefattyacidsinthebloodcauseinsulinresistance,resultinginareducedabilityofglucosetoenterbodytissues,includingthemuscleandliver.Theaccumulationofglucoseinthebloodisreferredtoashyperglycemia,andpersistenthyperglycemiaduetoinsulinresistancecanleadtosignificanthealthcomplications,includingelevatedriskforthedevelopmentoftype2diabetes,heartdisease,highbloodpressure,elevatedcholesterol,excessiveweightgain,obesityaswellasmanyformsofcancer.

Insulin resistance is common in individuals with obesity or type 2 diabetes (T2D), in

which circulating insulin levels are frequently increased. Recent epidemiological and

clinical evidence points to a link between insulin resistance and cancer. The mechanisms

for this association are unknown, but hyperinsulinaemia (a hallmark of insulin resistance)

and the increase in bioavailable insulin-like growth factor I (IGF-I) appear to have a role

in tumor initiation and progression in insulin-resistant patients1.

Inshort,insulinresistanceisapotentriskfactorforthedevelopmentofmanychronichealthconditions,whichcancausesignificanttissuedamageinboththeshortandlongterm.

Insulin Resistance Underlies Type 1 Diabetes Mostpractitionersbelievethatinsulinresistanceisonlypresentinindividualswithtype2diabetes,andthatpeoplewithtype1diabetesareinsulinsensitive.Thiscouldnotbefartherfromthetruth.Themechanismsthatcauseinsulinresistanceinpeoplewithtype2diabetesareidenticaltothemechanismsthatoccurinpeoplewithtype1diabetes,howeversincemanypeoplewithtype1diabetesremainleanthroughouttheirlife,theyareoftenviewedas“insulinsensitive.”Itisimportanttounderstandthatinsulinresistancecannotbeseenfromtheoutside,itisametabolicstatethatcanonlybemeasuredbythebalancebetweencarbohydrateandinsulin.

Oneofmyfavoritepapersofalltimetodescribethephenomenonofdiet‐inducedinsulinresistanceinpeoplewithtype1diabetesstatesthefollowing:

Current guidelines for intensive treatment of type 1 diabetes base the mealtime insulin

bolus calculation exclusively on carbohydrate counting. There is strong evidence that

free fatty acids impair insulin sensitivity. We hypothesized that patients with type 1

diabetes would require more insulin coverage for higher-fat meals than lower-fat meals

with identical carbohydrate content.

This evidence that dietary fat increases glucose levels and insulin requirements

highlights the limitations of the current carbohydrate-based approach to bolus dose

calculation. These findings point to the need for alternative insulin dosing algorithms

for higher-fat meals and suggest that dietary fat intake is an important nutritional

consideration for glycemic control in individuals with type 1 diabetes22.

Inanotherpapertoinvestigatetheeffectofeitherdietaryproteinordietaryfatonglucoseconcentrationsfollowingameal,theauthorsstatethefollowing:

Meals high in protein or fat increase glucose excursions in youth using IIT from 3 h to 5

h postmeal. Protein and fat have an additive impact on the delayed postprandial

glycemic rise. Protein had a protective effect on the development of hypoglycemia23.

Anotherstudyinpeoplewithtype1diabetesfoundasimilarresult,inthatamixedmealcontainingahigherfat‐proteindoseelevatesglucoselevelsinthebloodimmediatelyfollowingameal,resultingintheneedforadual‐wavebolusfromaninsulinpump.

Our study [in people with type 1 diabetes] examines the hypothesis that in addition to

sugar starch-type diet, a fat-protein meal elevates postprandial glycemia as well, and it

should be included in calculated prandial insulin dose accordingly. The goal was to

determine the impact of the inclusion of fat-protein nutrients in the general algorithm

for the mealtime insulin dose calculator on 6-h postprandial glycemia. A mixed meal

effectively elevates postprandial glycemia after 4–6 h. Dual-wave insulin bolus, in which

insulin is calculated for both the carbohydrates and fat proteins, is effective in controlling

postprandial glycemia24.

Anothergroupfoundthatcertainfeaturesofmuscleandliverinsulinresistancearespecifictopeoplewithtype1diabetes.Inastudycomparing25peoplewithtype1diabetesagainst25non‐diabeticindividuals,theauthorsconcludedthefollowing:

Insulin resistance in liver and skeletal muscle was a significant feature in type 1 diabetes.

Nevertheless, the etiology of insulin resistance was not explained by body mass index,

percentage fat, plasma lipids, visceral fat, and physical activity and was also not fully

explained by hyperglycemia25.

Insulin Resistance Underlies Type 2 Diabetes Itisverywellclassifiedthatfattyacidscauseinsulinresistanceinhumans,andthiseffectismostwidelyacceptedinpeoplewithtype2diabetes.Thefollowingparagraphdoesagreatjobofsummarizingtheconnectionbetweenelevatedfattyacidsoninsulinresistance:

Although insulin resistance is a key component of several chronic syndromes associated

with obesity such as type 2 diabetes mellitus and metabolic syndrome, the involved

factors and their underlying mechanisms linking excessive adiposity to insulin resistance

were not completely elucidated yet2–6. Evidence suggests that fatty acids, whose

circulating levels are markedly increased in obesity and associated-diseases, might play

a role in the development of skeletal muscle insulin resistance5,6. In this sense,

prolonged exposure of skeletal muscle and myocytes to high levels of fatty acids leads

to severe insulin resistance7,8. Among the different types of fatty acids, saturated long-

chain fatty acids such as palmitic and stearic acids were demonstrated to be potent

inducers of insulin resistance4,9. Several mechanisms have been suggested by us4,2,10,11

and others7,5,12–14 to explain how saturated fatty acids impair insulin actions such as the

Randle cycle, accumulation of intracellular lipid derivatives (diacylglycerol and

ceramides), oxidative stress, modulation of gene transcription, inflammation and

mitochondrial dysfunction. In the present review, we discuss evidence supporting the

involvement of these mechanisms in the regulation of insulin sensitivity by saturated

fatty acids and propose the mitochondrial dysfunction found in conditions of elevated

fatty acid levels has a central role in the pathogenesis of insulin resistance15.

Whenexcessfataccumulatesitthemuscleandlivertissue,theabilityofglucosetoenterbothtissuesiscompromised.Inresponse,thepancreassecretesanincreasedamountofinsulinto“push”theglucosefromthebloodintothemuscleandliver.Thisisaconditioncalledhyperinsulinemia,andwhenexcessiveinsulinproductionoccursovermanymonths(andsometimesmanyyears),theisletcellsinthepancreaseventuallyburnout,resultingintype2diabetes16.

Thiseffectofisletcell“suicide”isreferredtoasapoptosisinbiology,andoccurswhentheisletcellisnolongercapableofoverproducinginsulintomeettherequirementsofmuscleandliver.Ineffect,theisletcellbecomesexhaustedandcannolongerkeepup.Notonlyistheisletcellbeingaskedtosecretemoreinsulinthanitcanhandle,theaccumulationoffatwithintheisletcellitselftriggersthissuicidalbehavior17–20.Theauthorsstate:

An overaccumulation of unoxidized long-chain fatty acids can saturate the storage

capacity of adipose tissue, resulting in a lipid ‘spill over’ to non-adipose tissues, such

as the liver, muscle, heart, and pancreatic-islets. Under these circumstances, such

ectopic lipid deposition can have deleterious effects. The excess lipids are driven into

alternative non-oxidative pathways, which result in the formation of reactive lipid

moieties that promote metabolically relevant cellular dysfunction (lipotoxicity) and

programmed cell-death (lipoapoptosis)19.

Isletcellapoptosisisahallmarkoftype2diabetes,butalsooccursintype1diabetesasaresultoftheautoimmunedestructioninitiatedbythehost’simmunesystem.

Inobesesubjects,freefattyacidlevelsinthebloodareoftenelevated.Elevatedfreefattyacidlevels(duetoadiethighinfat)impairtheabilityofglucosetoentertissuesbypreventinginsulinreceptorsinthemuscleandlivertoallowforglucosetoenterthetissues.Inaddition,theliverrespondsbyoverproducingandexportingglucoseintotheblood,toprovidefuelforthebrain.

Inanotherpaperinvestigatingtheeffectoffatoninsulinsensitivity,theauthorsstatethefollowing:

Elevated FFA levels (due to obesity or to high-fat feeding) cause insulin resistance in

skeletal muscle and liver, which contributes to the development of T2DM, and produce

low-grade inflammation, which contributes to the development of atherosclerotic

vascular diseases and NAFLD (non-alcoholic fatty liver disease)21.

Toooften,theblameisplacedoncarbohydratesandnotonexcessivefatconsumptionandexcessivefatstorage.Itisimportanttounderstandthattype2diabetesisnotcausedbyexcessivecarbohydrateconsumption,rathertheaccumulationoffatthatpreventedglucosefromleavingtheblood.

How to Reverse Insulin Resistance Themosteffectivemethodofreversinginsulinresistanceistoconsumeadietlowinfattyacids,toalleviatethestressplacedonmuscleandlivertissueduetotheexcessaccumulationoffattyacids.Inotherwords,whentheliverandmuscleaccumulatefatovertimeduetoahighfatdiet,theylosetheirabilitytorespondtoinsulineffectively.Theonlywaytorestoretheabilitytorespondtoinsulinistoeliminatethestoresofexcessfattyacidswithinthemuscleandliver31.Thiscanbedonebyonethreemethods:

Method1:Burnexcessfatinmuscleandliverbyfrequentexercise

Method2:Reduceexcessfatinmuscleandliverbyeatingalowfatdiet

Method3:BurnandreduceexcessfatinmuscleandliverbyfrequentexerciseANDalowfatdiet

Obviously,method3isthemosteffectiveofthethree,howevereitherexerciseoralowfatdietarehighlysuccessfulmethodsofaccomplishingthesametask:getridofexcessfatinliverandmuscletissue.Asthesetissuesburntheiraccumulatedfat,normalinsulinresponsiveness(insulinsensitivity)isrestored,reducinginsulinrequirementsoverall.Thisisexactlywhyeliminatinginsulinresistancedramaticallyreducesinsulinrequirements–becauseasmallamountofinsulincansignalglucosetoentertissuesonceagain.

References Forallthereferenceslistedhere,visitwww.pubmed.org,andcopyandpastethetitleinordertoreadtheabstractorreadthepaper,iffreelyavailable.

1. Arcidiacono,B.etal.InsulinResistanceandCancerRisk:AnOverviewofthePathogeneticMechanisms.

Exp.DiabetesRes.2012,(2012).

2. Hirabara,S.M.etal.Time‐dependenteffectsoffattyacidsonskeletalmusclemetabolism.J.Cell.Physiol.

210,7–15(2007).

3. Silveira,L.R.etal.Updatingtheeffectsoffattyacidsonskeletalmuscle.J.Cell.Physiol.217,1–12(2008).

4. Hirabara,S.M.,Curi,R.&Maechler,P.Saturatedfattyacid‐inducedinsulinresistanceisassociatedwith

mitochondrialdysfunctioninskeletalmusclecells.J.Cell.Physiol.222,187–194(2010).

5. Shulman,G.I.Cellularmechanismsofinsulinresistance.J.Clin.Invest.106,171–176(2000).

6. Roden,M.Howfreefattyacidsinhibitglucoseutilizationinhumanskeletalmuscle.NewsPhysiol.Sci.Int.J.

Physiol.Prod.JointlyInt.UnionPhysiol.Sci.Am.Physiol.Soc.19,92–96(2004).

7. Griffin,M.E.etal.Freefattyacid‐inducedinsulinresistanceisassociatedwithactivationofproteinkinase

Cthetaandalterationsintheinsulinsignalingcascade.Diabetes48,1270–1274(1999).

8. Yu,C.etal.Mechanismbywhichfattyacidsinhibitinsulinactivationofinsulinreceptorsubstrate‐1(IRS‐

1)‐associatedphosphatidylinositol3‐kinaseactivityinmuscle.J.Biol.Chem.277,50230–50236(2002).

9. Yuzefovych,L.,Wilson,G.&Rachek,L.Differenteffectsofoleatevs.palmitateonmitochondrialfunction,

apoptosis,andinsulinsignalinginL6skeletalmusclecells:roleofoxidativestress.Am.J.Physiol.

Endocrinol.Metab.299,E1096–1105(2010).

10.MassaoHirabara,S.etal.Palmitateacutelyraisesglycogensynthesisinratsoleusmusclebyamechanism

thatrequiresitsmetabolization(Randlecycle).FEBSLett.541,109–114(2003).

11.Hirabara,S.M.etal.Acuteeffectoffattyacidsonmetabolismandmitochondrialcouplinginskeletal

muscle.Biochim.Biophys.Acta1757,57–66(2006).

12.Randle,P.J.,Garland,P.B.,Hales,C.N.&Newsholme,E.A.Theglucosefatty‐acidcycle.Itsroleininsulin

sensitivityandthemetabolicdisturbancesofdiabetesmellitus.Lancet1,785–789(1963).

13.Roden,M.etal.Mechanismoffreefattyacid‐inducedinsulinresistanceinhumans.J.Clin.Invest.97,2859–

2865(1996).

14.Brehm,A.etal.Increasedlipidavailabilityimpairsinsulin‐stimulatedATPsynthesisinhumanskeletal

muscle.Diabetes55,136–140(2006).

15.Martins,A.R.etal.Mechanismsunderlyingskeletalmuscleinsulinresistanceinducedbyfattyacids:

importanceofthemitochondrialfunction.LipidsHealthDis.11,30(2012).

16.Savage,D.B.,Petersen,K.F.&Shulman,G.I.DisorderedLipidMetabolismandthePathogenesisofInsulin

Resistance.Physiol.Rev.87,507–520(2007).

17.Unger,R.H.Lipotoxicityinthepathogenesisofobesity‐dependentNIDDM.Geneticandclinical

implications.Diabetes44,863–870(1995).

18.Shimabukuro,M.,Zhou,Y.T.,Levi,M.&Unger,R.H.Fattyacid‐inducedbetacellapoptosis:alinkbetween

obesityanddiabetes.Proc.Natl.Acad.Sci.U.S.A.95,2498–2502(1998).

19.Kusminski,C.M.,Shetty,S.,Orci,L.,Unger,R.H.&Scherer,P.E.Diabetesandapoptosis:lipotoxicity.

ApoptosisInt.J.Program.CellDeath14,1484–1495(2009).

20.Unger,R.H.&Zhou,Y.T.Lipotoxicityofbeta‐cellsinobesityandinothercausesoffattyacidspillover.

Diabetes50Suppl1,S118–121(2001).

21.Boden,G.Fattyacid‐inducedinflammationandinsulinresistanceinskeletalmuscleandliver.Curr.Diab.

Rep.6,177–181(2006).

22.Wolpert,H.A.,Atakov‐Castillo,A.,Smith,S.A.&Steil,G.M.DietaryFatAcutelyIncreasesGlucose

ConcentrationsandInsulinRequirementsinPatientsWithType1DiabetesImplicationsforcarbohydrate‐

basedbolusdosecalculationandintensivediabetesmanagement.DiabetesCare36,810–816(2013).

23.Smart,C.E.M.etal.Bothdietaryproteinandfatincreasepostprandialglucoseexcursionsinchildrenwith

type1diabetes,andtheeffectisadditive.DiabetesCare36,3897–3902(2013).

24.Pańkowska,E.,Błazik,M.&Groele,L.Doesthefat‐proteinmealincreasepostprandialglucoselevelintype

1diabetespatientsoninsulinpump:theconclusionofarandomizedstudy.DiabetesTechnol.Ther.14,16–

22(2012).

25.Bergman,B.C.etal.Featuresofhepaticandskeletalmuscleinsulinresistanceuniquetotype1diabetes.J.

Clin.Endocrinol.Metab.97,1663–1672(2012).

26.Woerle,H.J.etal.Mechanismsforabnormalpostprandialglucosemetabolismintype2diabetes.Am.J.

Physiol.‐Endocrinol.Metab.290,E67–E77(2006).

27.Firth,R.G.,Bell,P.M.,Marsh,H.M.,Hansen,I.&Rizza,R.A.Postprandialhyperglycemiainpatientswith

noninsulin‐dependentdiabetesmellitus.Roleofhepaticandextrahepatictissues.J.Clin.Invest.77,1525–

1532(1986).

28.Rizza,R.A.Pathogenesisoffastingandpostprandialhyperglycemiaintype2diabetes:implicationsfor

therapy.Diabetes59,2697–2707(2010).

29.Bock,G.etal.ContributionofHepaticandExtrahepaticInsulinResistancetothePathogenesisofImpaired

FastingGlucoseRoleofIncreasedRatesofGluconeogenesis.Diabetes56,1703–1711(2007).

30.Cline,G.W.etal.Impairedglucosetransportasacauseofdecreasedinsulin‐stimulatedmuscleglycogen

synthesisintype2diabetes.N.Engl.J.Med.341,240–246(1999).

31.Delarue,J.&Magnan,C.Freefattyacidsandinsulinresistance.Curr.Opin.Clin.Nutr.Metab.Care10,142–

148(2007).

32.Ley,S.H.etal.Associationsbetweenredmeatintakeandbiomarkersofinflammationandglucose

metabolisminwomen.Am.J.Clin.Nutr.99,352–360(2014).

33.Noto,H.,Goto,A.,Tsujimoto,T.&Noda,M.Low‐CarbohydrateDietsandAll‐CauseMortality:ASystematic

ReviewandMeta‐AnalysisofObservationalStudies.PLoSONE8,(2013).

34.Lagiou,P.etal.Lowcarbohydrate‐highproteindietandincidenceofcardiovasculardiseasesinSwedish

women:prospectivecohortstudy.BMJ344,e4026(2012).

35.Fung,T.T.etal.Low‐carbohydratedietsandall‐causeandcause‐specificmortality:TwocohortStudies.

Ann.Intern.Med.153,289–298(2010).

36.Rosenfalck,A.M.,Almdal,T.,Viggers,L.,Madsbad,S.&Hilsted,J.Alow‐fatdietimprovesperipheralinsulin

sensitivityinpatientswithType1diabetes.Diabet.Med.J.Br.Diabet.Assoc.23,384–392(2006).

37.Fuhrman,J.TheEndofDiabetes:TheEattoLivePlantoPreventandReverseDiabetes.(HarperOne,2014).

38.Fuhrman,J.Eattolivetheamazingnutrient‐richprogramforfastandsustainedweightloss.(Little,Brown

andCo.,2011).

39.Barnard,N.D.Dr.NealBarnard’sProgramforReversingDiabetes:TheScientificallyProvenSystemfor

ReversingDiabetesWithoutDrugs.(Rodale,2006).

40.Barnard,N.D.etal.Alow‐fatvegandietandaconventionaldiabetesdietinthetreatmentoftype2

diabetes:arandomized,controlled,74‐wkclinicaltrial.Am.J.Clin.Nutr.89,1588S–1596S(2009).

41.Barnard,N.D.,Katcher,H.I.,Jenkins,D.J.A.,Cohen,J.&Turner‐McGrievy,G.Vegetarianandvegandietsin

type2diabetesmanagement.Nutr.Rev.67,255–263(2009).

42.Craig,W.J.Healtheffectsofvegandiets.Am.J.Clin.Nutr.89,1627S–1633S(2009).

43.Trapp,C.B.&Barnard,N.D.Usefulnessofvegetarianandvegandietsfortreatingtype2diabetes.Curr.

Diab.Rep.10,152–158(2010).

44.Turner‐McGrievy,G.M.etal.Changesinnutrientintakeanddietaryqualityamongparticipantswithtype2

diabetesfollowingalow‐fatvegandietoraconventionaldiabetesdietfor22weeks.J.Am.Diet.Assoc.108,

1636–1645(2008).

45.Tuso,P.J.,Ismail,M.H.,Ha,B.P.&Bartolotto,C.NutritionalUpdateforPhysicians:Plant‐BasedDiets.

Perm.J.17,61–66(2013).

46.Jenkins,D.J.A.etal.Type2diabetesandthevegetariandiet.Am.J.Clin.Nutr.78,610S–616S(2003).

Cyrus Khambatta, PhD, Nutritional Biochemistry Mangoman Nutrition and Fitness, LLC

Mangoman Nutrition and Fitness | Facebook | Twitter | Yelp

Vegan, Avid Athlete, Type 1 Diabetic, Mango Addict

ABOUT THE AUTHOR

Dr. Cyrus Khambatta, PhDNutritional Biochemistry

At a young age my family recognized that I had a voracious appetite and seemingly bottomless digestive system. I’m not a very large guy - I’m 5’11” and I weigh 160 pounds, but I’ve always been able to outeat my size. Considerably.

As a young child I never paid attention to the quality of my food, I simply ate to satiate my taste buds and the tingling in the bottom of my stomach. It all caught up to me at the age of 22, when I was diagnosed as a type 1 diabetic overnight. It flipped my world upside down.

At that time in my life I didn’t understand anything about diabetes, I only knew that it had “something to do with sugar.” In the first year of life as a diabetic, my health deteriorated rapidly, to the point where I began to seriously question whether I would be able to exercise ever again. Constant lethargy, dehydra-tion, muscle soreness, and a lack of motivation occupied most of my waking day, and it was the most un-comfortable feeling I had ever experienced. By a long shot.

I changed my diet from the ground up by focusing on eating a diet high in plant-based carbohydrates, and in a short period of time I experienced abundant energy, high quality sleep, reduced blood glucose, increased athleticism, and a significant increase in my quality of life. One thing was blatantly obvious:

I’ve always been a huge advocate of food. And I’ve always had a voracious appetite.

Eating a large quantity of high quality fruits and vegetables every day is one of the

simplest and easiest paths to impeccable health

Vegan, Athlete, Type 1 Diabetic, Mango Addict

ABOUT THE AUTHOR

Reversing the Effects of Insulin ResistanceVia Research-Based Nutrition and Exercise

and fitnessnutritionmangoman

facebook.com/mangomannutrition

Follow Me on Facebook

The recipes in this book are a culmination of 10 years of experimentation. I sincerely hope you enjoy them and the abundant health they provide.

I earned a PhD from UC Berkeley in 2012, and have devoted my professional career to helping others understand the truth behind plant-based nutrition and fitness. I am a coach for those seeking better health, and specialize in reversing the effects of insulin resistance to control blood sugar in the setting of diabetes. My clients acheive exceptional health.

My goal is to teach the fundamental principles of what it means to live a TRULY healthy lifestyle, and to inspire you to take full control of your health using evidence-based nutrition information.