Lisse (Geluidsfragment uitspraak (info / uitleg)) is een plaats en gemeente in de Nederlandse provincie Zuid-Holland. De gemeente telt 22.655 inwoners (1 april 2016, bron: CBS) en heeft een oppervlakte van 16,11 km² (waarvan 0,41 km² water). Binnen de gemeentegrenzen liggen de buurtschappen genaamd De Engel en Halfweg.
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Vlag van Lisse Keer prediabetes só om - RSGplus
Gepubliseer op 15/10/2018. 15/10/2018
Wat is die verskil tussen prediabetes en diabetes?
Dié verdere gesprek volg om verwarring wat steeds bestaan oor diabetes, pre-diabetes, oorgewig en Banting bestaan, te probeer opklaar.
Wat is die verskil tussen pre-diabetes en diabetes? Kan pre-diabetes omgekeer word? Wat is die verskil tussen insulien-sensitiwiteit (voorheen genoem insulien-weerstandigheid) en pre-diabetes? En waar pas oorgewig en Banting in? Marí Hudson praat met prof. Tess van Merwe, ‘n endokrinoloog, om verwarring oor dié siektes en kwessies op te klaar.
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Enkele feite oor prediabetes
‘n Mens word met prediabetes gediagnoseer as jou HbA1c tussen 5,7 en 6,4 % is. Jou HbA1c dui aan hoeveel glukose aan jou Hemoglobien A (in jou roobloedselle wat suurstof dra) gebind is, en dui jou gemiddelde plasma glukose-vlakke van die voorafgaande 8 ntot 12 weke aan (ondat rooibloedselle se leeftyd 8 tot 12 weke is). Normale HbA1c vlakke moet minder as 5,6% wees. As dit hoër is as 6,5%, moet verdere toetse gedoen word om ‘n diagnose van tipe 2 diabetes te bevestig.
As daar ‘n skielike onverwagse piek in ‘n mens se glukosevlakke is, beteken dit nie jy het diabetes nie. Tipe 2 diabetes kan slegs met behoorlike toetsing gediagnoseer word. (Luister op 31 Oktober na Gesondheid op RSG, wanneer ons presies verduidelik hoe tipe 2 diabetes gediagnoseer word en wat dit beteken. Dit blyk dat alle dokters nie dié nodige toetse doen nie, en tipe 2 diabetes op raaiwerk ‘diagnoseer’.)
Mense met prediabetes se beta-selle in die pankreas produseer steeds insulien, maar hul insulien-sensitiwiteit is swakker is wat dit behoort te wees, wat beteken die beta-selle moet harder werk sodat die minder sensitiewe insulien steeds die werk van insulien kan verrig.
Prediabetes kan omgekeer word, omdat die beta-selle in die pankreas nog nie beskadig is nie. Maar as dit nie vinnig en daadwerklik omgekeer word nie, het die persoon ‘n vier keer groter kans om Tipe 2 diabetes te ontwikkel.
Prediabetes word nie met anti-diabetes middels behandel nie, maar deur gewigsverlies en oefening. Studies wat oor ‘n tydperk van 4 jaar op groepe pasiënte met prediabetes gedoen is, het onteenseglik getoon dat leefstyl-veranderings wat lei tot so min as ‘n 7% gewigsverlies en 150 minute se oefening per week (dus 30 minute 5x per week) tot ‘n 58% afname in jou risiko om diabetes te ontwikkel, lei. Terwyl behandeling met anti-diabetes medikasie soos Metformin tot ‘n afname van 28% in risiko lei.
Die beste eetplan is ‘n eetplan waar sowat 50% van jou totale energie-inname (kilojoules/calorieë) afkomstig is van lae GI koolhidrate (nie verfynde suikers, wit brood ens nie, maar wel volgraanprodukte), kosse ryk aan antioksidante soos bessies, goeie kwaliteit proteïene (nie gesprosesseerde vleis soos weense worsies, salami ens nie, en onthou dat vis – veral makriel, tuna, sardiens, forel en salm – en peulgroente goeie proteïenbronne is) en baie groente, veral groen en kool-groente. Klik hier vir ons Doen Dit Net aksieplan.
Eers as die pasiënt met prediabetes ná ‘n jaar van die leefstylveranderings (gewigsverlies, oefening en vermindering van stressors), nie daarin kon slaag om prediabetes om te keer nie, word middels soos Metformin saam met die leefstylveranderings ingespan. Medikasie word nie sommer van die begin af aaanbeveel nie, omdat medikasie tog newe-effekte het en nie naastenby so effektief is as leefstylveranderings nie; sommige kan lei tot ‘n Vitamien B tekort, en ander het effekte op die maagdermkanaal.
Stressors wat verminder moet word om prediabetes te help omkeer, is:
– ongesonde slaappatrone met te min slaap (minder as 8 tot 9 ure per nag)
– chroniese stres, omdat langdurig verhoogde kortisolvlakke die werking insulien letterlik teenwerk. (Toets jou stres-vlakke. Klik hier.)
Vroue met ‘n BMI groter as 40 (rofweg sowat 30 – 40 kg bokant jou ideale gewig), vroue wat tydens swangerskap diabetes ontwikkel het, of aan bykomende siektes ly, word met groter aandag en meer noukeurig opgevolg, en het ‘n verhoogde risiko om tipe 2 diabetes te ontwikkel. (Lees meer oor die BMI)
Die hoë vette en proteïene van die Banting eetplan is giftig vir die pankreas-, hartspier- en lewerselle
In ons eerste gesprek oor diabetes, het ons die nuwe navorsingsverslag oor Banting en koolhidrate in die eetplan bespreek.
‘n Onlangse verslag wat navorsing saamvat en in die gessaghebbende Lancet Mediese Joernaal gepubliseer is, het onteenseglik getoon dat eetplanne bestaande uit lae koolhidrate, (en dus meer diereproteïene en dierevette) nie die antwoord vir goeie gesondheid is nie. Prof Tess van der Merwe het die verslag in Monitor bespreek, maar dit is duidelik dat luisteraars meer inligting verlang.
Prof Tess van Merwe verduidelik in meer besonderhede wat die bevindings van die verslag is, wat foutiewe data sowel as korrekte feite uitwys, en bespreek dus ook Banting, diabetes, insulienweerstandigheid en obesiteit.
Luister hier na die program op Gesondheid op RSG.
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Interessante feite wat duidelik word uit die verslag
Die verslag is saamgestel uit inligting op meer as 15 000 mense, uit 18 lande op 5 kontinente en verskaf belangrike wetenskaplik-gegronde inligting wat oor 25 jaar ingesamel is. Die feite kan nie in twyfel getrek word nie.
Die verslag toon dat mense wat te veel koolhidrate (dieet met meer as 70% stysels en suikers) inneem, sowel as mense wat te min inneem (minder as 40% stysels en suikers) en dit met diereproteïene vervang (soos die Banting eetplan) skade aan hulle liggame doen, en dat hierdie eetplanne nadelig is vir gesondheid. Laasgenoemde eetplan verkort mense se lewens met gemiddeld 4 jaar.
Die gesondste eetplan is as 50 – 55 % van jou eetplan uit koolhidrate bestaan, en jy minder rooivleis en ander diereproteïene inneem en vervang met plantproteïene soos neute, grondboontjiebotter, avokado’s, peulgroente en so meer.
Wetenskaplikes verstaan ook waarom hoë vet en proteïen-inname gevaarlik is vir die mens se gesondheid; dit word die lipotoksiese model genoem wat vet om en in die hart, lewer, pankreas en spiere aanpak en dié organe bekadig. Sodra jy minder as 50% koolhidrate en meer dierproteïene/vette inneem, verander die metaboliese bane in jou liggaam en maak jou liggaam vier maal meer vetselle (120 miljoen vetselle of meer), vind ‘n ander energieverbrandingsproses in die selle plaas (bekend as vryvetsuur-oksidasie) en vorm ‘n waksagtige molekule in selle (lees meer oor sfigolipiede as jy belangstel). Die groot produksie van vet-stamselle wat tot die vorming van die massas nuwe vetselle lei, stimuleer die vorming van ‘n stof bekend as seramied uit die waks-selle. Seramied is ‘n gifstof wat die laaste insulien-produserende beta-selle in jou pankreas doodmaak. Seramied lei ook tot onreëlmatige hartspier-sametrekkings en beskadig die lewer.
In kort: te veel diervette (en die limiet is sowat die hefte as wat die gemiddelde verwesterde Suid-Afrikaner inneem) lei tot die vorming van meer vetselle, meer giftige seramied en vergiftig die pankreas, hart en lewer. Te veel diervette vergiftig onregstreeks lewensbelangrike organe.
Mense met ‘n BMI > 30 (rofweg 30kg bo jou ideale liggaamsgewig) plaas jou liggaam in die verkeerde metaboliese baan en verhoogde seramied produksie. Dit is noodsaaklik dat jou BMI < 26 moet wees. Gewigsverlies is absoluut noodsaaklik. Dit kan moeilik wees omdat jou brein as ‘n rekenaar optree en optree asof dit jou liggaam wil keer om jou gewig te verander, maar dit is belangrik dat jy moet vasbyt en jou brein-rekenaar dwing om te verander.
Wetenskaplikes gebruik nie meer die bewoording insulien-weerstandigheid nie, maar wel insulien-sensitiwiteit. Soos ‘n mens se insulien-sensitiwiteit verswak (en elke individu is anders afhangend hoeveel geen-mutasies betrokke is, wat weereens bevestig dat tipe 2 diabetes sterk oorerflik is), beweeg die mens van pre-diabetes na volbloed tipe 2 diabetes. Met volbloed tipe 2 diabetes het die mens nie meer werkende beta selle in die pankreas nie, kan dus nie meer self enige insulien vervaardige nie en benodig die pasiënt insulien- inspuitings. Voordat volbloed tipe 2 diabetes intree, word middels voorgeskryf wat insulien-sensitiwiteit verbeter. Ons sal in ‘n program op 10 Oktober meer verduidelik oor insuliensensitiwiteit, pre-diabetes en diabetes.
soos verskaf deur Prof Van der Merwe op haar blog en Facebook-bladsy.
I have had an overwhelming amount of requests for more/repeat information about the talk on RSG this morning regarding the low carbohydrate, high animal derived protein diets. Also popularly known as ketotIc diets. There are also requests regarding the watershed moment and importance of the publication in the Lancet, one of the most prestigious scientific journals in the world. I thought it best to break the information into small sections over the next week or two.
We are heading towards the world obesity week
The theme selected for this year and presented to the UN by World Obesity was to tackle all forms of discrimination against the disease of obesity. It is running under the ‘this too must fall’ campaign. For years I have expressed my views on the narrative used when talking about obesity or the patient suffering from this disease. Phrases like ‘if they just get up and move it will sort the problem’ or ‘what is wrong with their will power’, or the one I dislike most ‘you are lazy and gluttonous’. We would never dream of addressing a person with a dreaded disease like cancer in that manner, so why do we do it with obesity?
Since it causes more deaths per year than most other chronic diseases, it seems like there is something that is not adding up here. The answer is actually quite simple – it is the most ill understood and most exploited disease in the world. People and even professionals popping up everywhere with treatment strategies that as no scientific validity. Professionals that will bridge over from an unrelated medical field into obesity treatment, simply so that they can sell a book, or idea, or potion. ‘Afterall, these patients are desperate and will try anything’. We have to stop this. But I cannot do this alone. I need every bit of help. I therefore appreciate every word, every sentence and every gesture you make/take to help me to spread the word of rational sciences. Together we are so much stronger.
#1: First writing of a mini series on the low carb, high fat diet, also known as the ketogenic diets
A watershed publication appeared on the 16th of August in the very prestigous LANCET medical journal. The article, authored by Seidelmann and his collaborators addressed the topic ‘Dietary carbohydrate intake and mortality: a prospective cohort study and meta-analyses’. It is a highly powered longitudinal study that investigated 15000 free living subjects over 25 years. The study included 18 countries in 5 continents.The outcome was adjusted for age, sex, race, total energy consumption, diabetes, cigarette smoking, physical activity, income level and education.
Both high (more than 70%) and low ( less than 40%) percentages of carbohydrate diets were observed to increase mortality, with the least risk observed at 50-55% carbohydrate intake. Life expectancy decreased most in the less than 30% carbohydrate group where protein was sourced from animals. In this group life expectancy decreased by a staggering 4 years throughout life. E.g. for a 46 year old, life expectancy was decreased to 42 years.
Protein and fat derived from plant product in the low carbohydrate group resulted in a lesser effect, with life expectancy derceasing by 1.1 years. The high carbohydrate intake group (more than 70%) had a small but signifant increase in all cause mortality.
# 2: In the second post of my mini series on the adverse impact of the low carb, high protein/ high fat diet, I need to first address the control of body fat mass
Unless there is a scientific understanding of how the body functions, the public will always be at the mercy of cult groups, sensationalists, people that make idle promises and those who profess to be so learned and filled with knowledge, that they can fly in the face of all that is scientific.
Determination of body fat mass follows a brain centric model in the human. Not an isolated peripheral fat mass control model. So even though the function of fat storage and release of fat is to an extend excecuted by insulin, it is just another step in the much bigger and more complicated metabolism of determination of the body stat.
This brings us to two crucial principles that must be understood.
– Firstly, the body stat cannot be manipulated by moving macronutrients around. Extremes of intake, or no intake, of e.g. carbs or protein cannot overide the central control of appetite, satiety and energy expenditure. Various nuclei in the brain, together with the hypothalamus, will ultimately control your body stat.
– Secondly, insulin does not have some magical, isolated control of your fat mass. Statements such as ‘it is your insulin resistance causing your overweight problem’ or ‘ if we treat your insulin resistance your weight will improve’ is incorrect and a display of how little is understood about your overweight. Likewise statements that macronutrient shift can force your body to use fat as a fuel, is incorrect and a display of ultimate lack of knowledge of how metabolism works. Like looking through a keyhole and professing that you have seen the whole room.
# 3: In the third of my mini series on the low carbohydrate high fat high protein diet, I was going to pause a bit on how insulin works.
I have however noted that I have received many messages of people arguing that a ketogenic diet is a less that 5 percent content of CHO intake and therefor not applicable to the 40 percent quoted in the Lancet study. This urges the following.
– Firstly, that there is still a poor understanding that arguing about 5 or 40 percent is futile. Fat mass is controlled principally by the brain’s homeostatic powers and not by what happens at the level of the fat cell. Think of the process as an orchestra in which numerous instruments will be co-ordinated by the conductor, in this case very powerful signaling from the brain.
– Secondly, the Lancet article studied longevity and it indicated very powerfully that a less than 40 % CHO intake decreased survival. The main principal to understand is exactly that. Stop arguing about 5, 10 or 40 persent. Swing your head around the fact that low CHO is not the way to go, and do this by looking at the big picture. Respected sciences will look at the following: basic science research and evidence, clinical outcomes and dangers and longterm documented outcome. Clear your mind and now lets start from a clean slate.
With the increased insulin secretion of obesity, type 2 diabetes and excessive refined sugar intake (not CHO intake per se), insulin will act by storing excess intake in various metabolically active cells. At the earliest, lowest level of increase of insulin on the logarithmic scale, it starts with fat tissue and as the level increases will move to muscle and liver.
The next principal to understand is that this increase equates, at onset, normal physiology and that as long as you are still gaining weight you must be sensitive to some of the actions of this hormone. Elevated insulin levels does not equal insulin resistance! For practical purposes you can accept that insulin resistance has started at the first signs that your body is not handling glucose homeostasis any more.i.e. you have an elevated blood sugar that appears from time to time. Most patients will also give this history quiet accurately. ‘Doctor I have been at this weight for 2 years now. I may go up or down by 10 kg but I cannot keep it down’. It is because your brain has now stored your previous highest weight molecularly down to a half kilo and will defend that weight by brain centric control of metabolism and various other homeostatic mechanisms.These pathways are magnificently elegant and complicated in its execusion. At this point it can also be stated the concept of so called ‘food addiction’ is wrong and again a display of lack of insight into the brain’s mechanisms of control. In my next delivery more about what happens during increased insulin secretion and what is important to know.
# 4: In the fourth post of our mini series in the low carb high fat/protein diet I am going to deal with some research speculations
First I want to refresh your memory about some physiological functions insulin has. It is the hormone that will store fuel such as glucose in the fat cel, but also be inhibiting breakdown. This pathway forms part of normal physiology to prevent us from running into trouble. These two pathways are called lipogenesis and lipolysis and insulin is therefor also known as the most important, but by no means the only! anti-lipolytic hormone. It has been speculated that during weight gain, as well as excessive sugar and refined carbohydrate intake (more than 70% of intake), insulin secretion increases and less of the breakdown product named free fatty acid (FFA) will appear in the blood stream.
Some researchers have proposed that this lower level of FFA triggers a state of ‘cellular starvation’ that will cause a higher appetite and a slowing down of energy expenditure by for e.g. the liver and muscle. This will then conspire to driving obesity. Introducing a very low carb intake should then reduce insulin secretion, which in turn would lead to a supposedly higher rate of fat mobilizition and more oxidation of FFA and then your speculative weight loss will follow. Herein lies flaw number one. Fantastic and very sophisticated whole body FFA turnover studies done by icons in the field of metabolism such as Prof Keith Frayn from the UK and Prof Peter Arner from the Karolinska Institute in Sweden, have shown that FFA levels in obesity is HIGH, not LOW. So despite our knownledge that higher insulin levels will lead to more lipogenesis, what is seen in obesity is an almost rampant FFA turnover. In a condition such as diabetes associated with obesity we have double trouble. Both a HIGH FFA and a HIGH glucose. Extending this pure scientific logic, a very high fat intake will have its own load of glycerol and FFA to add to the pool. With no proven ‘cellular starvation’ theory present in obesity metabolism, combined with a high influx of saturated fat, we now have a recipe for disaster. Read more about this and flaw number two in the follow-up posts.
# 5: On the ongoing topic of insulin resistance
I often have patients coming to me stating that they were told their ‘bloods’ showed that they have IR. So herewith misnomer number TWO. It is unfortunate that the commercial labs started using formulae such as the HOMA and Quicks index in the same context as IR. These formulas are mathematically invented models for use in a research setting, losely signifying a diminshed SENSITIVITY of insulin to glucose. It is easy to see how the misusing of these indexes with IR started, because at a first glance they look the same! But they are not! For clinical use these indexes are totally useless!! and have no relevance to ‘what diet can be prescribed next’ to ‘fix it’…or far worse even, slapping the patient onto Metformin to ‘correct their IR’.
True IR can only be measured in a science laboratory with long and complicated clamp studies. Making use of the HbA1 as a clinical tool is far more useful, as a HbA1 of 5.7 to 6.4 indicates that you are pre diabetic. Outcome studies have shown a five fold progression to diabetes. So next time ask your doctor for your HbA1 level, forget about all the IR stories and forget about a diet that can ‘fix your IR’.
# 6: This will be post number six and my final say on the low carb high fat high protein diet
The South African public had been grossly mislead by this diet and it is time to stop this ridiculous fad. A high saturated fat intake has been shown to not only cause apoptoses of many cells, incuding the beta cell of the pancreas, but can also decrease the clearance of insulin in the liver.
This will lead to a drastic increase in insulin levels in the body to unacceptably high levels, as the liver is responsible for 40% of the clearance of insulin produced in the body. It will lead to overstimulation of the pancreas and eventually the beta cells will burn out and diabetes will ensue.
But more importantly, it will stimulate the homeostatic and hedonic feeding pathways in the brain towards feeding. Have you ever wondered how people who was on this diet, start overeating on fruit, carbs and other sweet things as soon as they come of this ridiculous diet? Well now you have the answer.
The brain has taken over and not in a good way.
Fortunately there is bariatric surgery for people with a BMI over 30 and have become enlightened enough to understand that you are not going to fix this mess with yet another round of diets. Alternatively you can embrace the DASH diet and very serious cognitative behaviour modification therapy at a good centre. The success of the last option for people who have suffered from chronic obesity will be less than 5% over 5 y. The success of metabolic surgery- 50 times that. Why? Because 80% of how these ops work would be by fixing what has gone wrong through altering hormonal signals to brain, hind gut, pancreas, liver and muscle.
Wat sê Prof Tim Noakes oor Banting: Lees en luister hier.
Diabetes is aan die toeneem
Die skok-feite oor die samestelling van The Secret Fat Burner
Vergeet van jou vrese oor Aspartaam: dit is veilig
Waar pas die DASH dieet in?
Besoek die webblad vir meer inligting: https://www.sasso-online.org/
Tags BantingGesondheid op RSGInsulienweerstandigheidTipe 2 Diabetes