natural treatments for diseases from diabetes

hello, i'm norman swan. welcome to this program in our serieson guidelines and type 2 diabetes. every year there areabout 3.8 million deaths globally attributable to diabetes. in australia, type 2 diabetes isthe fastest-growing chronic disease, with the total number of australianswith diabetes and pre-diabetes estimated at a whopping 3.2 million, and it's the sixth-leadingcause of death. this program looks at two nhmrcevidence-based guidelines that are new

and address complicationsand comorbidity in type 2 diabetes. they are the evidence-based guidelinesfor diagnosis and management of kidney disease in type 2 diabetes, and the guidelines for the managementof diabetic retinopathy. for those of youwatching on your computers, you can type your questions directly into the studio. just click on the livetalk tab at thetop of the web page you're looking at. that also means, of course,that we can ask questions of you. here's one to get you going:

click away on that one, and we'llgive you results of that in a moment. as usual, there are a numberof useful resources available on the rural health educationfoundation's website: now let me introduce our panel to you. stephen twigg is an endocrinologistat the university of sydney and presidentof the australian diabetes society. - welcome, stephen.- good evening. alan cass is the senior director of the george institutefor international health,

and director of the pocheindigenous health centre at the university of sydney. - welcome, alan.- good evening, norman. paul mitchell isprofessor of ophthalmology at the university of sydney,and runs the blue mountains eye study. - welcome, paul.- thanks, norman. good to be here. and david guest is a rural generalpractitioner in goonellabah in nsw. - welcome.- thanks, norman. david, challenging,

dealing with comorbiditiesin general practice, i assume. it's a growing area. it's a bigger and bigger problem. it's something that's takingmore and more of gps' time. if you get systems in place, you canprobably cope with the challenge. talk to me about the trendsthat are going on, stephen. as you've mentioned already,diabetes is on the rise. we believe that approximately100,000 people per year in australia are developing diabetes.

it's very similarto the worldwide trend. there are a number of factors thatare probably critical in the process in terms of the development of diabetes. the prevalence changesin different groups in australia? yes, there are certainlyhigher-risk groups, particularly an ageing population. there are certain ethnic groups that are at higher risk than others. there are also issues

to do with lifestyle change. as we can see on this slide - this data is from the turn of the millennium - approaching a million people, or 7.4% of adults aged over 25 had diabetes in australia at that time, well over 90% of it being type 2 diabetes. the other conditions, impaired fasting glucose and impaired glucose tolerance,

or as you referred to them, the pre-diabetes conditions, also extremely common. so approaching one in four australian adults have some form of glucose abnormality. norman: extraordinary. it's a remarkable figure. norman: it's also age-dependent?

yes, very much so. if we dissect this out further, the same study, the ausdiab study, demonstrated a strong age-dependence for diabetes, indicating that the ability of the pancreas to produce insulin tends to deteriorate with time. approaching one in four australian adults in their 70s will have diabetes

in comparison to a much lower percentage of people earlier in their life. we're trending upwards fasterthan we thought? very much so. world health organisation data,recent trends have suggested, rather than seven million peopleper year developing diabetes, it's more like ten million people. we're going to hear about thatin the more recent estimates, in the next year 2010 datafrom the international

diabetes federation and who. norman: this graph shows we're tracking faster than we thought. and the australian data, very similar. in the ausdiab study, whilst 'e' on the far rightis an estimate based on previous decades, in the last decade, the late '90s, then into the 2000s,

the figures are well above what the estimates were on the trend line. a study from the australian institute of health and welfare 2006 indicated it's more like 1.5 million people who have diabetes, then increasingly, 100,000 a year. so really, even off that scale, if we look at more recent estimates

of diabetes in the australian community. we're talking here about absolute risk,global risk, just as muchas we're talking about glucose? definitely. glucose, if you like, is the marker. people with diabetes havetwo- to fourfold the rate of cardiovascular diseaseas the general community. as you've pointed out, it doesemphasise global cardiovascular risk and the importance of tightblood pressure and cholesterol control.

david, on the day of broadcast,yesterday's medical journal of australia described the fact thatgeneral practitioners are not measuring absolute riskto the rate they should be. what are the barriersto measuring absolute risk? it's a gp-education problemto start with. there are tools available nowthat make it much easier. i have a preference for a computerisedelectronic health record. getting data out of the computer makesthese sort of assessments much easier. a website which i think is the onerecommended by various colleges

to assess absolute cardiovascular-disease risk is available on the web and available on the desktop.that's a very useful tool for gps. you've got an example of this risk toolthat's in the guideline? that's right, norman. if we look at the next slide,this is an example. this is for people with diabetes. the charts are divided into thosewith and without diabetes. people with diabetesare a high-risk group. they can be stratified on the basisof their cardiovascular risk

in terms of looking attheir systolic blood pressure, their cholesterol,hdl total cholesterol, hdl ratio, gender status and smoking status. it's possible then to identify whether a person would be deemedat a high cardiovascular risk, in which case the intensity of themanagement of their surrogate markers - their blood pressure, their cholesterol,their glucose and also antiplatelet therapycan be modified appropriately. norman: you're arguably more likelyto save their life

by managing those other factorsthan their sugar? it's not one or the other,but it's both. all of them are important. for example, diabetic retinopathyglucose is the major factor that will contributeto that complication. in terms of cardiovascular diseasein people with diabetes, the risk is probably approaching 15%to 20% of the variation in risk will be glucose, depending uponthe degree of glycaemic control. and cholesterol and blood-pressurecontrol, very important in that setting.

how important, paul, are theseother risk factors than glucose? we know that glucose controlcan help diabetic retinopathy, but those other risk factors? - there's growing evidence, isn't there?- that's right. the effect of good diabetesglucose control on preventing the developmentand progression of diabetic retinopathy has been shown both in type 1and in type 2 in the ukpds. that latter study, ukpds, actually demonstrated almostan equivalent effect in type 2 diabetes

of blood-pressure management. indeed, recent studies, the accord studies and the rass study,just recently published, have shown that in factreally tight blood-pressure control, perhapswith modern blood-pressure agents, arbs, can actually reduce the incidenceof diabetic retinopathy and may result in regressionof existing retinopathy lesions. and in kidney disease, alan cass? again, the key factors to controlare blood pressure.

also, how well you control glycaemiais a key factor in terms of progressionof kidney disease. norman: what's the management challenge,stephen? diabetes, as we know,is extremely challenging. there's the combination of lifestylemanagement and pharmacotherapy. there's the importance of vigilancewith respect to diabetes management, because, as we know, targets canbe difficult to maintain over time. when we look at the optimisationof care, in terms of patient care, we have tight blood pressure,blood glucose and cholesterol targets

monitoring for complications. this slide indicates that in general,we will achieve a lot if we have a generic,crowd-based approach. if we go on to the one which shows themanagement challenge to optimise care, once we can assess cardiovascular riskfor the individual and we can target more appropriatelylipids and blood pressure and glycaemia for the particular person -the career stage of their diabetes - then we can expect to achieveeven better outcomes when we customiseor individualise the care.

whilst the world is obsessedwith obesity, it's not the whole story? definitely not. we have these other major risk factors,we have to target those. we try and bring our waists inand reduce body weight if not stop it going higher, but there's a lot we can do to preventend-organ damage from diabetes. alan, you've got a lot of experienceworking with indigenous communities. indigenous rates of type 2 diabetesand complication rates are enormous. is it a different disease or just worse?

i think the evidence is thatit's not a different disease, that the issues of poverty,poor access to care, a whole series of factors come together that make the same common problemsof diabetes and related chronic illnesses worse rather than an entirely differentapproach being needed. what are the targetswe should be aiming for? the racgp has generic targets,as shown here - glycaemia, total cholesteroland blood pressure.

in general, these will work well forpatients and for health professionals. so, the a1c target,less than or equal to 7%. total cholesterol, less than 4. these days, we focus on ldl cholesterol,less than 2.5, if not down to 2. then blood pressure,less than or equal to 130/80. however, if we do customiseor individualise it for the personwho has significant proteinuria, we want a tighter blood-pressure targetthan that. people with knownischemic heart disease,

we want a tighter ldl cholesterol level- less than 1.8. and depending upon the stageof the person's diabetes, early on we know thattight glycaemic control can reap rewards decades down the track. there's even quite a pushfor hba1c levels 6% to 6.5% early on after the diagnosis. that's controversial. if you look at the most recent type 2diabetes guidelines for glycaemic control, whichyou might address in subsequent weeks -

i know we're not addressing thosetoday - the generic targets,a1c, less than 7.0%, and we know we can achieve thatfor a lot, if not all, of our patients. we can achieve it for a lot. there's increasing data,again from accord and advance and vadt, a number of studiesover the last 18 months, 2 years, that early on in the diagnosis -and also from the ukpds follow-up - early on, we need to aim for very tightglycaemic control, get in early. we know that in general,

type 2 diabetes is a delaying diagnosisof four to five years between when it developsand when it's diagnosed. we're missing years therewhen we can help achieve tight control of these surrogate markersfor our patients. paul, you've been following this groupof people in the blue mountains for many years,many of whom have diabetes. getting them earlymakes a difference? absolutely. in fact, one of the messagesthat has come out in the last year is this issue of metabolic memory.

so, good control of diabetesin the first period of diabetes is really important. it's been shown in the ukpdsin type 2 diabetes that good diabetic controlover the period of the study persisted, despite the fact thatthe haemoglobin a1c levels in intensive versus routine control... we've got a graph to that effectto show. that metabolic memory effectwas shown initially in the dcct and is now being shown in ukpdsfor retinopathy

and for other complications. that probably tells uswhere the challenge is. we know that on average,we're picking people up with diabetes several years afterthe diabetes is established. for primary careand the health system generally, what can we do to opportunisticallypick up people? for example, coming each year, most australians do attenda general practitioner's at least once. there is strong evidencein the australian context

that if we opportunistically screen50- to 69-year-olds for diabetes, we can pick it up earlierand intervene and prevent heart attacks, strokesand premature mortality. are you doing that, david?putting you on the spot. yes, probably indirectly. a lot of patientshave lots of blood tests. you'll flip through and see that the sugars are in the 6sor occasionally higher, and it behoves us to concentrate on thatand get a fasting glucose,

get a two-hour glucose-tolerance testdone and see where we're up to. just take us through quicklythe algorithm to remind us of the basic managementof the glycaemic side of things before we move on to the complications. the algorithm involvesintensive lifestyle management. that is both the diet and regular physical activity. we do find in most people as time goes on

they do require pharmacological agents in addition to focusing on lifestyle. in terms of the hba1c targets that will help determine what type of additional medications are needed and when, following the initial lifestyle intervention, metformin is our first-line agent. it certainly is effective

at lowering blood-glucose levels, has a relatively low side-effect profile, well tolerated, and on top of that, in the ukpds we've referred to, had good outcomes in terms of cardiovascular and microvascular outcomes. subsequent to that though,

as time goes on, hba1cs often deteriorate and people need more than metformin alone. sulphonylureas in australia for decades have been our second port of call. then, multiple third-line options. each of the third-line options will sit on that line because they are newer agents

which might be less well studied than sulphonylureas, or they have challenges associated with them, for example, injections, as in the case of insulin. norman: we've got the results of your first poll question. we asked where you were located: here are the findings.

16% evenly split between metropolitan,regional and remote. and that big one, the blue one,is rural. welcome to you all. it's good to see such an even splitand an appropriate split in terms of your location. i'm going to ask the second questionnow, which is: so, we'll get your answers to thatwhile i ask david guest, what is the general practiceannual cycle of care when you've got somebody with diabetes?

with patients with established diabetes, it's a protocolwith which to manage them. it involves clinical measuresthat we probably should do every time we see the patient,but certainly six-monthly, you need to check the blood pressure, the weight and hopefully the feet, but that's sometimes something we don't get around to. annual tests needed,

hba1c certainly annually, more frequently depending on the level of control. we want to know what the lipids are doing, and hdl in particular in relation to some new risk-factor calculators. with diabetic nephropathy, we want to keep an eye on

the albumin in the urine. there's also the necessity for second-yearly eye examination, either yourself or more commonly where i come from, with optometrists and ophthalmologists. keep on eye on the social factors - smoking, alcohol, exercise, diet areas. if you get yourself into

a regular pattern with that, either on your own or with the help of your team, you can keep your diabetic patient under control. take us through the issues in terms of chronic kidney disease. chronic kidney disease is commonin diabetes. chronic kidney disease ismanifest evidence of kidney damage.

the way that this is picked up is eitherthrough a simple blood test, then estimationof the glomerular filtration rate, where the gfr is less than 60mlper minute, evidence of significant kidney damage. the other way is through picking up protein leakageinto the urine - microalbuminuria - through to more overt nephropathy. when we think about howwe measure these things in terms of the serum creatinineon one hand,

how much protein in the urineon the other hand and the estimation of gfr,it's sometimes complex. some of the keys to be cognisant ofis that often leakage of albumin into the urine,microalbuminuria, is one of the earliest markers. this usually occurs whensomeone has normal renal function. norman: how best to measure that? there are different waysin which that's measured. ways that are felt to be equally valid

would be a spot,particularly morning urine for albumin-creatinine ratioor a timed urine collection, again, looking for albumin. we were originally trainedin terms of 24-hour urines, but in terms of common usein primary care, both of those methods are commonly used. norman: that should be part - of the annual cycle of care?- yes. today's patients expectfasting blood tests,

so during the urine test at the sametime has become part of the protocol, part of the routine. so that's... you've knocked off a lot of your kidneysbefore your creatinine rises. absolutely right. that's the way to pickit up early, focusing on the albumin. a key thing with the creatinine,a common measure - we do it on many patients - is that you might have losthalf of your kidney function before you get an abnormally elevatedcreatinine measure.

that's where the simple calculationof the estimated gfr, which is done routinely by labsthroughout australia now, will provide a more ready measure of the amountof renal dysfunctional damage. why are we interested in that? both of those are important. both the level of albumin in the urineand the level of kidney dysfunction are known predictors of eventsfor people with diabetes. in other words, chronic kidney diseasepredicts heart attacks and strokes.

correct. why are we interested?it's very common. from ausdiab, perhaps a quarterof people with diabetes have evidence of chronic kidney disease. and of all peoplewith chronic kidney disease, what's the diabetes in relation tothe cause for end-stage kidney disease? diabetes is now the leading cause ofend-stage kidney disease in australia and in similar countriesthroughout the world, and interestinglyalso in developing countries. that relentless drive of diabetescontributing to end-stage kidney disease

is quite clearin the australian context. the advance studyrelated cardiovascular disease risk with albuminuria and renal disease. absolutely correct. the advance study was a large,randomised-control trial with over 11,000 type 2 diabetics looking at blood-pressure controland glycaemic control. there is quite clear evidence there that both of these markers are

predictors of heart attacks and strokes and progression of kidney disease to renal death or dialysis. both independently and together, they add one to the other, so people at highest risk are people with reduced kidney function and significant albumin leakage in urine. norman: do they go hand in hand?

they do go hand in hand. the figure that one in four peoplewith diabetes probably has some early kidney diseaseis about the figure for retinopathy. it used to be thought that retinopathyoccurred before kidney disease. that's before we measured kidney diseaseproperly. we know that once kidney diseasereally starts to accelerate, retinopathy really gets a hold onparticularly macular oedema. people,as their creatinine starts to rise, that's when we see retinopathy,if it hadn't already needed treatment,

really become aggressive. because they're parallel processesaccording to severity? probably a parallel process, but certainly peoplewho have got significant proteinuria have a major increased riskfor macular oedema. what are the other risk factorsfor diabetic retinopathy? the principal risk factor isglycaemic control, but in type 2 diabetes,it looks like blood pressure control is probably almost or as important.

lastly, blood lipid controlmight also be important. data from field studies suggests that an aggressive approach to blood lipidsmight also be helpful, although that's not so solid. we certainly know that elevated lipids are associated withmacular oedema specifically. the nice thing about that is,it's blood pressure and glycaemic control that are also related to progressionof kidney disease.

so similar approaches to management ofthese factors that complicate diabetes can reap the rewards in terms of keeping people's visionand keeping their kidney function. how reversible is diabetic retinopathy? it's quite reversiblein the early stages. the recent data on this came from the... got a blank on the study?it'll come to you later. one of the most recent study of arbs showed that if you had retinopathyat the first two stages,

microaneurysms only or a fewmicroaneurysms and retinal haemorrhages, those stages were reversible withreally tight blood-pressure control. but once the retinopathy becameslightly more advanced than that, then it was not reversible. these are the direct study findings. we'll come back to do moreon diabetic retinopathy in a moment. i've got the answerto the poll question, which is: the red is six-monthly, and it's 27%. 18% said it depends on the patient.

54.5% said annually. what's the right answer,professor twigg? stephen: i would say annually,but it depends on the patient. you're happy with both? you've got a thinking physician there.i'd prefer a thinking physician any day. annually is the cycle of care. norman: so most peoplehave got it right. as is recommendedin the nhmrc guidelines, which stephen co-wrote.

just testing, just testing. we've talked about screening,just to go back to kidney disease. we've talked about the test that you do. what about albumin-excretion rates? what validity does that have? people use both albumin-creatinineratios and albumin-excretion rates in screening for damage to the kidneycausing albumin leakage into the urine. both are tests that are validand have good sensitivity and specificity in terms oftheir role in screening

and measuring response to therapyfor diabetics. what are confounderswhen you're doing urine tests? it's critical that there are a numberof key confounders. urine infection, menstruation in women, people who might have exercisedsignificantly in the preceding 24 hours. many australianswho eat high-protein diets, these people will have artificiallyelevated readings, for example, and some medications,for example nonsteroidals and others that are commonly taken.

when you're talking aboutblood pressure control, are we talking about angiotensinreceptor blockers and ace inhibitors or others work as well? the answer is both. yes, there is accumulating evidencefrom a number of trials that for people who have, in terms of prevention of earlychronic kidney disease in diabetes and people with early stagesthat ace inhibitors and arbs might have a particular protective role.

as well as that, it's the overall levelof blood pressure control. indeed,there now seems to be added evidence that even for peoplewho are normotensive with diabetes that there is the same benefit as people with any levelof blood pressure in lowering their blood pressurein terms of kidney disease, for example. as you implied earlier, paul, similar findings nowfor diabetic retinopathy? certainly the ukpds didn't differentiatebetween different blood pressure agents,

and there's never really beenfantastic data suggesting that one class of blood pressurelowering medication would be better. recent studies of ace inhibitorsand arbs seem to show the best effects, but there hasn't beena head-to-head comparison. stephen? i agree. you look at all the nationaland international guidelines and first-line for hypertensionfor people with diabetes is an ace inhibitor or arbs.

as paul and alan mentioned though, the critical issue istight blood pressure control. lipid control is not as strongbut still worth doing? lipid control is important, because people with diabeteshave high cardiovascular risk. there is not strong evidence that lipid control prevents progressionof kidney disease. but they are at high riskof heart attack and stroke, therefore require good lipid controlin that context.

david, were you going to say something? just agreeing that at the macrovascularlevel, that's what you're looking for. the place of aspirin in patients? does aspirin help with kidneyor eye disease? here we go. put on your seatbelts.we're in for a rough trip now. perhaps i can address the issueof lipids. no, let's have the aspirin question.professor twigg? for secondary prevention,there's no question antiplatelet therapy is critically important,

and that gets back tothe cardiovascular link. you've got to have an eventbefore you start the aspirin - for it to be of benefit?- yes. for primary prevention, this is where cardiovascular risk tablescan be extremely helpful. if a person is deemedto be at high risk, you'd be prone to use antiplatelettherapy. i would under those conditions. norman: but there's no evidence for it.- that's for cardiovascular protection. there is, but you have to extrapolate.

there was the hypertensionoptimal treatment study, which had 1,700 with type 2 diabetesin it, but they're only 10% of that population. aspirin worked very well there. there was also the physicians'health study for primary prevention. from a cardiovascular point of view,there's a basis for using aspirin under those conditions. it is complex in people with diabetes. there's some evidence that maybeaspirin resistance occurs -

resistance to the action of aspirin. and what is the correct dosage? from the point of viewof kidneys and eyes, we'll move on to my esteemed colleagues. but from the cardiovascularpoint of view, tables can be helpfulfor antiplatelet therapy. i'll come back to paul'cause i so rudely interrupted him. to go on the aspirin point, one of the original diabetic retinopathystudies, the etdrs,

looked at whether aspirin was beneficialfor people with diabetic retinopathy. it really showed no benefitover no aspirin. of course, in people who needed aspirinfor cardiovascular reasons, there was no contraindicationto giving aspirin because there wasno increase in haemorrhages, even in people with severe retinopathy. there was no increasein vitreous haemorrhage. so it's safe, but there areno protective effects on its own. can i add to that?

stephen talked about the hot trial. there was a recent analysis, presented this yearat the world congress of nephrology, showing that people in that trialwho had chronic kidney disease - people we're talking about here with chronic kidney diseasein the context of diabetes - had the greatest absolute benefit fromaspirin therapy of the entire group. because they're at much highercardiovascular risk. even though they had some increasein some risks,

the added benefit in terms ofthe prevention of, in that case, heart attack and vascular eventsoutweighed that. so people with ckd hadparticular benefit from aspirin therapy. and smoking cessationaffects the kidneys and eyes? smoking has been looked at a lotin terms of retinopathy, but no good data suggests that cessationof smoking benefits retinopathy. norman: so smoke doesn't getin your eyes? i'm sure it does, and it's great to stopif you've got diabetes. it gets in your eyes from maculardegeneration rather than anything else.

- what about kidneys?- there is evidence people who smoke are at greater risk of progressionof chronic kidney disease. what about protein restrictionwith grade 3 renal disease? i wouldn't advocate that now. that was something... so generations of peoplewith impaired kidneys have been eating that horrible stuffall that time? correct. the evidence of benefit is that it might at best delay the onsetof dialysis by one or two months.

and you feel every month of that. the clinical care guidelinesare very helpful here in terms of the pointsthat paul has raised about aspirin not being a riskin terms of intercurrent retinopathy. they are nicely coveredin the guidelines, and as alan points out,the smoking issue too. even the executive summary, i'd encourage people to go onlineand have a look at it. excellent marketing, professor twigg.we're most impressed.

what about salt reduction in kidneydisease? does that have any benefit? salt reduction is becoming increasinglyan issue of focus in australia. in general we eat a high-salt diet. a lot of that is about not saltthat we add but that salt is in... ..takeaway foods and foodsthat we buy at the supermarket. it's quite clear that the high-salt diethas implications for hypertension. therefore, i think it will be an areaof increasing focus - how can we reduce that in terms of interactionwith the food industry, for example,

so we can lower blood pressure? that will be very relevantfor management of diabetes. a question from new south wales - 'what is the incidence of chronic kidneydisease with gestational diabetes?' maybe i can answerthe gestational diabetes part, then pass on to the colleaguesfor chronic kidney disease. gestational diabetes by definitionis diabetes that develops in pregnancy, then usually resolvesshortly afterwards. you wouldn't expect kidney diseasewith it?

yes. it does affect about 5%of the pregnant population. after saying that, pregnancy-inducedhypertension and pre-eclampsia and eclampsia, they do cosegregatewith gestational diabetes, probably through body weightand equivalent risks. in terms of renal disease per se, in some of the renal disease-relatedconditions, there is some link. i'll stop there and pass on to others. the actual riskof significant renal disease at the time of gestational diabetesor pre-eclampsia, for example, is low.

people who might already haveovert diabetic nephropathy at the time of becoming pregnant and high blood pressure and thingsare at more risk in that conditionof worsening of renal function and of having greater difficultyin managing those comorbid conditions. there are a lot of people interested infollowing people after having the pregnancy,having a baby, in terms of their then ongoing riskof developing type 2 diabetes and related chronic kidney disease,

where it does appear that there is,in long-term, some increased risk. another question is,'how does steroid abuse influence the incidenceof chronic kidney disease in existing type 2 diabetes?' i assume we're talkinganabolic steroid abuse here. that's not somethingi have any particular knowledge about. you haven't got many muscled-up... what about steroidsas in corticosteroids? there's obviously concerns about obesityand its interaction with diabetes

as to whether that's a risk factorfor development and progression of chronic kidney disease in diabetes. but again, it's not somethingthat features steroid use, in terms of developmentof chronic kidney disease. let's have a look atour first case study. back a while, back about 10, 11 years, i was working in the coal fields then. i went to the doctor because thediabetes had sort of caught up with us, the high blood pressure and that.

the doctor had taken blood testsand that and said, oh, yeah, there's something wrong withyour kidneys. so i had to go to townsville. they took a biopsy on the kidney.they thought it was a diseased kidney. they took a biopsy, and the result ofthat was, neither kidney was diseased. we had to go and see a dietitianin mackay when he came back. they said, don't eat this anddon't eat that. eat this and eat that. so he did it, but nobody ever said,you've got to follow it up. it wasn't until about five years agothat he started feeling down.

he said he was feeling a bit tireda lot. i said, you need a good sleep.stop eating so much. he got the flu.he was away working in a mine. he used to fly in and out.and then he got sick. he flew back in, and i couldn't believehe was a person when i opened the gate. i thought, what's wrong with you?he said, i'm really sick. jeez, it nearly killed me.it was just something unbelievable. that's when he asked his doctorif he could get his kidneys checked, and lucky he did do that.

next i know,i'm at the renal area of the doctor's. it just went from there. i knew something was wrong whenhe didn't come out. i kept seeing people going out,and i thought, something's wrong. then i thought, oh, no. when i walked in and saw the faces,i knew then. it just hits you like a brick. it all happened so quick. it obviously was over a long periodof time.

probably the good life caught up. personally, it gets back to the wayyou're brought up, i guess. the foods that you eat whenyou're in your younger days, grog, everyone does it. a lot of people overindulge. it just depends. it gets back to your dietand the way you look after your body. i didn't show him,i'd just go out and cry. i couldn't handle it.

not only my father died,his father died of it. i've got aunties on my mother's sidethat have died of it down in south australia. so you think, he's got it,so i must have it. it knocked the whole lot of us.really knocked the family. the grandkids just couldn't believepoppy could get sick, not their poppy. not a good story there, david. no, no.like he said, it happened so quick,

but it really is somethingover a decade or more, isn't it? i think it's probably a good idea whenwe have patients with diabetes early on that we have our registers set upso we can keep track of them. it would be even betterif we could negotiate some plan on how we're going to manage itaccording to the cycle of care so they don't get away from us. and using a team. and using a team to ease the burden,particularly on rural gps who don't have much time.

he looked as if he was trucking alongwith a haemoglobin of about 9. i think that's right. they talk about the devastating impactof diabetes and kidney disease on the family. the key issue is multiplemissed opportunities for engagement in the management of the diabetes. he talked about all the factorswe know are crucial - his blood pressure, diet, all of the approaches to managementthat could have made a difference

and prevented his severe kidney failure. this problem is writ largeagain and again across the country. i'm going to ask you another question. how would you rate your understanding ofcorrelation between serum lipid levels, good blood glucose controland blood pressure control and eye complications? it's probably a bit better since we'vebeen speaking about it for a while. let's see how you rate it now. while you're answering those questions,we've got another case study to watch.

let's look at darren's story. my name's darren dorey. in september, i'll be 43. i live in warrnambool,in the south-west corner of victoria. it's approximately 300kmor three hours from melbourne, a little seaside town that isa nice, little friendly community. i was diagnosed with type 2 diabeteswhen i was 27. i was told to change diet, and i was put on some tablets.

but as time went byand i didn't feel any different, i got more and more slack with it. probably for the next ten years,i lost focus on control of the diabetes. at the time i was told,you have to have your eyes checked. ok, well, that's pretty serious. i drive a truck for a living,so i've got to keep on top of the eyes. after a couple of years of going,yep, your eyes are fine, you stop worrying about it. around about 2001

i was starting to struggle a little bitwith seeing some road signs. i went in to the optometrist'sto get some glasses. she had a look in my eyes and said,you've got a massive bleed in the eye. she said, you need laser surgeryand you need it now. i walked outof the ophthalmologist's rooms after having something like 300, 400shots of laser in the eye. i ended up having a vitrectomy. probably 18 months later,i developed a cataract, which i had out in about 2006,in the left eye.

that brought back vision beautifully. it was like, wow, a whole new world.this is all good. in 2007i'd actually gone back to truck driving. i guess going back into trucks was, for the diabetes,one of the worst things i did. i did a lot of travel whereyou'd take off for a few days' trip and forget to take your medicationswith you. i noticed it was getting harderto read the paperwork, and the headlights of cars startedto become more glarey -

the lights would flare. i thought, i'd bettergo back to the ophthalmologist. he looked at my eyes and said,'are you still in sales?' i said, 'no, i'm a truck driver.' he just said, 'not anymore you're not.hand in your licence tomorrow.' i then had to go home to my wifeand four kids and say, 'i don't have a job, and it looks likei might be going blind.' the same day,our landlord called over to mention that he'd put the house on the marketand we'd have to move.

yeah, life just crumbled. paul mitchell, entirely preventable? i think that blindness from diabeticretinopathy should be preventable. there really should not be any cases of people who go blind from this diseaseanymore. there are still people going blindfrom it, and there will still be some people. but if you look at every oneof those cases, you can really detect what went wrong.

clearly, in the early stages of hisdiabetes, he was poorly managed. he put his head in the sand. maybe his doctors didn't impress on him the absolute importanceof having regular checks, but it should have been prevented. after he had that first lot of therapy,it looks like he again lost contact. he should have had pretty intensefollow-up after that first therapy. but he didn't go,and he went back to driving again. if you look at darren's story, there aremany circumstances where really,

the wrong path was taken, andhis blindness, or severe vision loss, could have been prevented. how do you screen your patientsfor retinopathy, david? do you send them to the optometrist? i send them off to the optometristor ophthalmologist, probably a 50/50 split, or a bit moreto the ophthalmologist where we are. question from michael stuckeyin queensland - 'why not annual retinopathy screening?'paul? it's been looked at.

around the world, most diabetesassociations recommend annually, but in fact, the developmentof retinopathy occurs relatively slowly. it's been shown that two-yearly isactually sufficient. if someone hasdifficult-to-control diabetes, if they've already gotother complications, of course they needto be seen more frequently, even if they have no retinopathy. how good are the screening tests? this is ophthalmoscopy?

yeah, this is ophthalmoscopy. the eye doctor, or optometrist, wouldn'tuse a handheld ophthalmoscope. he would use a slit lampwith a much wider area, being able to screen the retinamuch more effectively than the handheld ophthalmoscope. we also have the potential availability for clinicsof non-mydriatic photography. this is what they're using in someaboriginal communities? that's right. that's very effective.

you see a blown-up picture,you can immediately see if there are any retinopathy lesions. the standard though, at the moment,would be pupil dilation? yeah. the standard is pupil dilatation,then examination of the retina by someone who can do it properly - an ophthalmologist, an optometristor a well-trained gp or physician. what are the criteria for referralto an ophthalmologist? certainly non-ophthalmologistscan manage people with diabetes in terms of retinal screening

until the point at which any significantretinopathy is present - anything more than the occasionalhaemorrhage or microaneurysm. from that point people shouldsee an ophthalmologist. marisa pilla from north queensland asks, 'is there any ace inhibitorthat's superior to the others in helping to prevent retinopathyor the worsening of the condition?' we don't know. there are two recent studieslooking at two different arbs and they both showed beneficial effects,

but there's beenno head-to-head comparison. she also asks about antioxidants. the areds study suggested that a certain cocktail mighthelp macular degeneration. does it help in diabetic retinopathy? there's no evidence thatit helps diabetic retinopathy. talk us throughlaser photocoagulation here. there are some new therapies coming on when you've got microaneurysmsand bleeds.

once ophthalmologists take overfollow-up and management of people with diabetes, what they're really criticallyinterested in doing is evaluating the patient at an interval so that they would detectvision-threatening retinopathy and could apply laser treatmentat the optimal time. the indications for laser treatment arethe presence of either new vessels, and this is an advanced stageof the background type of retinopathy. new vessels are fragile, they bleed,they don't really help,

they don't bring new blood to the area. the second is macular oedema. this is the more frequent andmore important complication to detect. that is harder to detectwith ophthalmoscopy. that's why you really needan ophthalmologist or optometrist to examine the patient. and the treatment of macular oedema? the treatment of macular oedema iscurrently laser treatment using the guidelinesthat have been around for 25 years.

it's reasonably effectivebut not brilliantly effective. certainly many people will stilllose vision. we now have some otheradjunctive therapies that can help. the main one is anti-vegf therapy. this is vascularendothelial growth factor. - this is like avastin or lucentis.- that's right. these agents are an adjunct to therapy. they don't do away withthe need for laser, but they can help to dry out the macula

until laser treatmentcan be a bit more effective. laser treatment is probablymore effective if it's applied when the macular oedema is resolved. and the role of fluorescein angiography? becoming less and less. fluorescein is not a particularlypleasant test to have done. we actually do it very rarely. we might do it at the onset, before we start laser treatmentfor macular oedema, once,

but we rarely repeat it these days. we don't do it at all for screening or for the follow-up of peoplewith diabetic retinopathy. unlike retinal detachment,vitrectomy has a different reason. you're trying to get rid ofthe haemorrhage from the vitreous? there are two circumstances. the first is to get rid ofthe haemorrhage and scar tissue, because new vessels that bledwill then develop scarring, and that scarring will cause tractionon the retina.

because retinal detachmentis increased in diabetes? correct, and it's a tractional typeof retinal detachment. the other type of needfor vitrectomy surgery is for traction on the macula itself, which can cause macular oedemato persist and be chronic. but we are doing less and lessvitrectomies now because physicians are managing peoplewith diabetes much better. we're seeing less peoplepresented at act v, scene iv, and we're needing to doa lot less vitrectomy surgery.

just to explain, the vitrectomy involvesmicrodissection to remove scar tissue. correct. it involves usually two portson the side of the eye with instrumentation which can dissectand peel off membranes and coagulate blood vessels. people have said that doing cataractsurgery can also damage the retina. what risks are therein cataract surgery and diabetes? this is an important issue,and it's still important. we know that people with diabetesdevelop cataract much earlier than people without diabetes.

there's a direct effect of glucoseon the lens in the eye. the type of cataract they getis a cortical cataract - the spokes when you dilate the pupil - you can see them quite easilywith an ophthalmoscope - or an opacity on the back of the lens. the problem is that when peoplewith diabetes develop cataract, they may also be developing retinopathy. if there is any early macular oedemaor moderate retinopathy, then you can develop macular oedemaafter cataract surgery,

perhaps as a response tothe inflammation of the surgery itself. one of the issues thatall ophthalmologists know is that we must stabilisethe retinopathy before cataract surgery as much as we possibly can. what about access togood ophthalmological care when you're living ina small country town? this is always difficult. ophthalmologists liketo live in the nicer suburbs, and don't necessarily go to the countryso often.

but in all country areas in australia,there is some degree of access. it always needs to be better,but there is reasonable access. and if there isn't,you need to let us know so the college of ophthalmologistscan look at this. local ophthalmologistsin some of the larger rural areas will be preparedto travel to smaller areas if they think there's a reasonable need. this non-mydriatic screening canbe transmitted for people to look at. correct. right now there's anotherapplication to the medicare group

to consider fundingnon-mydriatic photography. this would produce a fantastic wayof screening people. it meansthey wouldn't have to travel a long way to see an optometrist or eye doctor. gps themselvescould read the photographs quite well with relatively minor training. that has not yet been approved,but we're hoping it will be. let's have a look at darren's storyagain, and what his life is like now. my left eye hasbeen left with 25% vision.

the right eye, about 10%. the hardest thing with the eyesis that they see totally differently. i describe it as being likethe old fun mirrors at luna park, where everything is distorted, or fog up your windscreen,jump in your car of a cold morning, going for a drivewithout a clean windscreen. then put a few little linesand black dots into your line of vision then go cross-eyed so you've gotdouble vision on top of that. i was never actually told

about the correlation between diabetesand depression. if my sugar levels were high,my moods would swing. but once i lost the sight, thedepression came in like a tidal wave. it became all-encompassingto the fact where i attempted suicide. i lost all self-esteem,i lost all self-worth. it cost me my marriage. i haven'tseen my children for two years. october '07, my life fell into a hole -a very, very deep black hole. it took me another six months to crawlmy way out of it and restart my life. one of the biggest things that helped meget my life back on track,

or helped me out of the holethat i was in, i made an appointment to see my gpand couldn't get in, so they said, we've got another doctorhere with an appointment open. do you mind seeing someone else? i said, i just need a script,so that would be great. i sat down with this new female doctor.very young, she was. she had a look at my file and said, you haven't had this test done fora while. you haven't had this test. what's going on here?what's going on there?

we'd better take control of this. it was almost a light-bulb momentfor me, like, someone is listening,someone is taking note. the gp i was seeing,we had a good rapport, but it just became the usual, yep, i've run out of tablets.can you help me here? it was in and out, script in hand,thanks very much, see you later. she also linked me in withthe local psychiatric services through the local hospital,and i was given a case manager,

who, once again,showed a lot of compassion and care and was listening to me. also vision australiareally came on board and helped mewith a lot of adaptive stuff. they sent out a personto help me learn how to walk again. it sounds silly, but you learn to feelthe ground rather than see the ground. i couldn't see the normal,everyday things anymore, simple things like how to put somethingin the microwave, push the button to go. i couldn't see that button.

i couldn't feel that button'cause they're flat-panel. vision australia said, we've got these dots,put them on the go and stop buttons. i can't read how many minutesi've got up, so i count how many times it beeps. it's just one of the little thingsyou take for granted that suddenly become an issue. it was the supports behind methat helped me. i'm now employed bysouth west healthcare,

psychiatric services department. vision have come down from melbourneand put in a program which helps with email,it enlarges the font automatically. i can't read normal-size font. also, enlarged keys or enlarged stickerson the keyboard. without them, i've got no hope. the main thing for someonewho's new to diabetes, or even a doctor that'streating a new diabetic, is to emphasise what it isand how it works.

doctors need to emphasise,you won't feel it coming. as i said earlier,i expected to have signs. if there's any damage, i expectedto have the signs of it coming. you don't feel it coming. it creeps up very, very slowlyuntil suddenly it's out of control. a lot of the things i did was, ifit's serious, they'll tell me about it. of course they thinkyou've understood it, so they let it go. suddenly it becomes a huge issuedown the track. i honestly feel,if it had been more of a team effort

between my gp and myself,maybe i wouldn't have lost the sight. tragic, david. david: yes. you feel bad as a gpwhen you see a story like that. there's a place for having a registerof your diabetic patients and reviewing that regularly and getting your team to help youin the management of these patients and make sure they're not lostto follow-up and you can keep on them. i joke with our diabetes educatorwho visits our surgery

that we play good cop, bad cop. she tells them all the things theyhave to do, then i come in and say, sharon says this, so you'd better dothe right thing for next time. let me get the resultsof the poll question: 6% of you said you had no understanding.hopefully we've improved that tonight. 62% said you've got moderate,and 31%, comprehensive. so over 90% of you havegot a reasonable understanding, at least on a self-assessment basis. we won't be administering anymultichoice questionnaires tonight.

paul, not a good story there,but you're saying it's becoming rarer. it's becoming rarer. one of the pointswe could say about darren is that he's been throughthe gamut of therapy. usually their vision is stablefrom that point. usually there's no further progression, because the disease becomesrelatively quiescent after it's done all that damage. he probably will hold his visionfrom now on. we should be looking at his case andsay, this should have been prevented.

we really need to work hard to preventall these cases, and i think we can. we mustn't forgetthe psychosocial issues. depression goes along with it. it makes diabetes worse. absolutely.it's an important part of the package. we know people with diabetes have a two- to threefoldhigher prevalence rate of depression. it's a vicious cycle. what are your takeaway messagesfor the audience, david?

know who your diabetic patients are, and keep them under careful,close review. don't try and do it all yourself. your diabetes educators,dietitians, podiatrists, they're all there to help,and make sure the necessary gets done. - and get the targets right.- get the numbers right. paul? at least two-yearly,i review by competent examiner. make sure that you really work hard

at the control of diabetesblood pressure and blood lipids. - alan?- chronic kidney disease is common. it can be readily detected and followedwith simple blood and urine tests. and again, blood pressureand glycaemic control are crucial to preventing progression. for me, those two case histories show that too many peoplefall through the cracks. both as individualsin our own clinical practice and the health system generally,

we need to do something betterto prevent those disastrous outcomes. - stephen?- vigilance is key. diabetes does tendto be a progressive condition, and the complications. we need to get to know our patientswell. work with them as one of the key membersof the team. recognise that we can preventat many different levels. hopefully we can prevent many peoplefrom developing diabetes, many others from diabetes complicationsdeveloping

once they've been diagnosedwith diabetes. even those who develop more severelater-stage complications, there's a lot that we can do. never give up,prevent at multiple different levels and get to know your patient. thank you all very much.very interesting and very important. i hope you got a lot from the programtoo. the series of four programs we'remaking on type 2 diabetes guidelines will be available in december freeon dvd.

to order,visit the foundation's website. copies of the guidelines can bedownloaded from diabetes australia: www.diabetes.com.au. if you're obtainingeven more information about issues raisedin tonight's program, there are a number of resourcesavailable don't forget to complete and send inyour evaluation forms and register for cpd pointsby completing the attendance sheet. i'm norman swan.

from all of us, see you next time. funded by the australian governmentdepartment of families, housing, community servicesand indigenous affairs. captions bycaptioning & subtitling internationa�