Dr Sebastian Rushworth

Jaylee

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I read the paper and the studies it discussed seemed to involve T2s who were often early stage or even prediabetic. I'm not sure how much relevance these studies have to countries where T2s are typically supplied insulin at a late stage of diagnosis (ten years?) , other meds have been tried and failed, and quite possibly the T2's insulin own insulin production has been impaired by long term high bgs. I guess you can't really do a study for these people, because you can't leave a control group untreated.

Try low carb before giving insulin to a new T2? That seems pretty sensible to me. But it says nothing about using insulin to treat a long term T2 who has already run through a large number of other options.

And yes, it would be nice if doctors did more cpeptide tests to determine how much insulin new and old T2s were producing, if only because you could then spot a lot more misdiagnosed T1s and also spot the T2s whose production is failing.

I would argue that insulin is life saving for some T2 diabetics (or at least sight and limb saving).

It looks like a generalisiton to me. From a junior doc just picking the bones over an old study.. (23 year old?)
No other basis for insulin being prescribed from doctors other than it manages my BG.. Banting's vision. For T1D.

Regarding heart attacks or potential strokes? I don't get the "logic..?" If that's all this guy has got regarding alarming T2s. I'd rather scroll on.....

I'm just bemused non IDs successfully managing their own condition with a successful regime. Would be interested.?
 

Seacrow

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@lucylocket61 Adding more insulin to someone who is already overproducing will only increase insulin resistance. It may appear to be working by lowering blood glucose but sooner or later the patient will run out of road. Long term outcomes are not improved. They key point here is that endogenous production must first be measured, but it rarely is. If the patient is underproducing then insulin therapy has a valuable role. Otherwise it’s just kicking the can down the road.
If you're taking diabetes as a stand alone condition, then reducing insulin resistance rather than taking more insulin is a better option, I agree. Diabetes IME rarely comes without co-morbidities. Take me, normal insulin production, insulin resistance out the wazoo. I have tried so many things to reduce my resistance I have lost count, none work. I can
1) Eat reasonably and inject insulin
2) Eat low carb, put up with high blood glucose and organ damage
3) Eat the tiny amount my endogenous insulin covers and starve (malnutrition)

The important bit is, the insulin may just be postponing the problem, but it's causing no permanent damage while it does so. Maybe one of my other co-morbidities will someday get resolved, and then lowering my resistance will be possible.
 
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Seacrow

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Insulin is primarily a BG lowering drug. That's how it works.. That's why it was developed. Used & dosed correctly. It can be used to manage & why prescribed..
The information leaflet that comes with the insulin makes me laugh.
Potential Side Effects : Low blood glucose
Well duh! Although I would argue low blood glucose is the intended effect and hypoglycaemia is the side effect.
 
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Riva_Roxaban

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The information leaflet that comes with the insulin makes me laugh.
Potential Side Effects : Low blood glucose
It's similar to "may contain nut products ie peanuts" on food products.

I have never heard of the "doctor" either jut to keep on topic.

Edit: Deleted wrong medication warning.
 
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Jaylee

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The information leaflet that comes with the insulin makes me laugh.
Potential Side Effects : Low blood glucose
Well duh! Although I would argue low blood glucose is the intended effect and hypoglycaemia is the side effect.
Yarp, I hear you. that's how it can sometimes goes.. Geting the balance right regarding it's use & diet.

Easier said than done.. ;) Junior doctors need not comment.
 

bulkbiker

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please read the other articles by this person closely, he has some wild and unsubstantiated anti covid and conspiracy rhetoric going on based on spurious 'research'. Yes, I read around the blog.
So the poor guy can't win.. he quotes all the research but because he has a different opinion to you his evidence becomes "spurious" .
I've read almost all his stuff and have yet to find anything "spurious" about it... just well researched and well presented facts.
 

VashtiB

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Hi everyone- while the thread relates to an article looking at administered insulin for type 2 please continue to be respectful of those who do not share your opinion. In my personal opinion the most important thing is to have an approach to your health that is sustainable. For me that is very low carb. For others even very low carb may not be sufficient. For others it may not be sustainable to be very low carb. This site is intended to be informative and supportive. So discussion is helpful but please be respectful to those who do not share your opinion.
 

lucylocket61

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Be aware on this forum you are not allowed to imply insulin is bad, so Lucylocket61 may say her father gained a few years thanks to insulin, but I am not allowed to tell how my father, who was a type 1, died when he was only 43 years old.



Exactly, here is an interesting video on this topic:

Dr Benjamin Bikman | Foods That Help Lower Insulin & Reverse Diabetes | Cortisol Effects on The Body
I repeat: the use of insulin is very different for type 1 compared to type 2.

There are supportive and informative threads in this forum for insulin users of both types. Not threads telling type 2 diabetics to stop using insulin or saying it is bad. Why do you think it is bad?
 

Oldvatr

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I hope drs. know this stuff. I don't know how much insulin I should take. I don't think my dr. knows either. I rely on my meter numbers 4-11 as the safe range. I am type 2 as diagnosed.
As a T2D of some 30+ years now, I see my safe range as 4.5 - 7.2 mmol/l which I achieve most days now. i used to have an Hb/a1c of 106 when maxed out on meds (metformin 2000mg, Gliclazide 320 mg and Acrtos) I am now on 40 mg Gliclazide only + Low Carb diet with Healthy Fat) I am not an insulin user, but was considered to be a prime candidate before i took charge and behaved myself.
 

Antje77

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Be aware on this forum you are not allowed to imply insulin is bad, so Lucylocket61 may say her father gained a few years thanks to insulin, but I am not allowed to tell how my father, who was a type 1, died when he was only 43 years old.
I'm sorry about your father.
But if you are implying T1's shouldn't use insulin, this forum is the wrong place for you indeed.
T1's die without insulin, and giving dangerous medical advice or making suggestions that are unreasonable or impossible to implement is definitely not allowed on the forum. (C12, B10, A11 and C13)

Furthermore, this is a thread about T2. Further off topic discussions will be removed.
 

Dark Horse

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The author of the opinion piece linked to says this about the UKPDS trial, "3,867 people with newly diagnosed type 2 diabetes were randomized to either intensive blood sugar control with insulin, aiming at a fasting blood sugar of less than 6 mmol/l " whereas the original paper says, "3867 newly diagnosed patients with type 2 diabetes, median age 54 years (IQR 48-60 years), who after 3 months' diet treatment had a mean of two fasting plasma glucose (FPG) concentrations of 6.1-15.0 mmol/L were randomly assigned intensive policy with a sulphonylurea (chlorpropamide, glibenclamide, or. glipizide) or with insulin, or conventional policy with diet. The aim in the intensive group was FPG less than 6 mmol/L." In other words, he is claiming that all of the intensive treatment was with insulin whereas it was either with a sulphonylurea or with insulin.
https://www.researchgate.net/public...ons_in_patients_with_type_2_diabetes_UKPDS_33

He also doesn't seem to understand the natural history of retinopathy. He says, "It’s also worth noting here that most of the 3% reduction in microvascular disease was actually a reduction in probability of getting laser therapy to the retina, i.e. was not connected with any noticeable symptoms but rather with a treatment that was given based on opthalmoscopic findings (people with diabetes regularly have opthalmoscopic examinations of their retinas to look for signs of disease progression)." One of the difficulties with retinopathy is that people don't get symptoms until very late on in the disease - the damage has already been done. If people require laser treatment to prevent sight loss, then that is clinically significant. The percentages may seem small but when you scale up for the huge number of people with diabetes in this country, that is a lot of people who may have be able to avoid sight-loss.

The author also says, "Note also that the study wasn’t blinded, so it’s not beyond the scope of possibility to think that the researchers might have influenced events in such a way that the insulin treated participants got less laser therapy than the control group, in order to improve their stats. " However, in the original paper it says, "The clinical decision for photocoagulation or cataract extraction was made by ophthalmologists independent of the trial."

The opinion piece doesn't address the way that insulin is used in people with type 2 diabetes in later stages of the disease when natural insulin production has dropped.
 
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Jaylee

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The author of the opinion piece linked to says this about the UKPDS trial, "3,867 people with newly diagnosed type 2 diabetes were randomized to either intensive blood sugar control with insulin, aiming at a fasting blood sugar of less than 6 mmol/l " whereas the original paper says, "3867 newly diagnosed patients with type 2 diabetes, median age 54 years (IQR 48-60 years), who after 3 months' diet treatment had a mean of two fasting plasma glucose (FPG) concentrations of 6.1-15.0 mmol/L were randomly assigned intensive policy with a sulphonylurea (chlorpropamide, glibenclamide, or. glipizide) or with insulin, or conventional policy with diet. The aim in the intensive group was FPG less than 6 mmol/L." In other words, he is claiming that all of the intensive treatment was with insulin whereas it was either with a sulphonylurea or with insulin.
https://www.researchgate.net/public...ons_in_patients_with_type_2_diabetes_UKPDS_33

He also doesn't seem to understand the natural history of retinopathy. He says, "It’s also worth noting here that most of the 3% reduction in microvascular disease was actually a reduction in probability of getting laser therapy to the retina, i.e. was not connected with any noticeable symptoms but rather with a treatment that was given based on opthalmoscopic findings (people with diabetes regularly have opthalmoscopic examinations of their retinas to look for signs of disease progression)." One of the difficulties with retinopathy is that people don't get symptoms until very late on in the disease - the damage has already been done. If people require laser treatment to prevent sight loss, then that is clinically significant. The percentages may seem small but when you scale up for the huge number of people with diabetes in this country, that is a lot of people who may have be able to avoid sight-loss.

The author also says, "Note also that the study wasn’t blinded, so it’s not beyond the scope of possibility to think that the researchers might have influenced events in such a way that the insulin treated participants got less laser therapy than the control group, in order to improve their stats. " However, in the original paper it says, "The clinical decision for photocoagulation or cataract extraction was made by ophthalmologists independent of the trial."

The opinion piece doesn't address the way that insulin is used in people with type 2 diabetes in later stages of the disease when natural insulin production has dropped.

I maybe wrong.. But diabetic scan eye checks back then for retinopathy (1998?) which is what the blog is talking about, were just a Poleroid pics taken of the back of the eye.. (Looked like fuzzy pictures of Mars to me..) Then the two images stapled to a patient form & pawed over & discussed by an eye doc.. No high def digital imaging emailed at that time..? Been doing this stuff for 46 years..
 

Oldvatr

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I maybe wrong.. But diabetic scan eye checks back then for retinopathy (1998?) which is what the blog is talking about, were just a Poleroid pics taken of the back of the eye.. (Looked like fuzzy pictures of Mars to me..) Then the two images stapled to a patient form & pawed over & discussed by an eye doc.. No high def digital imaging emailed at that time..? Been doing this stuff for 46 years..
Did they have lasers in those days? I think that even now the photo's are not the prime diagnosis tool I had my scan last week, and the opthalmologist eyeballed me for some time before confirming diagnosis. I will need treatment some time, but not yet, and I am still able to drive. My problem is not diabetes related but is caused by a blocked cartoid artery following a stroke or two..

Seems the Doc is confusing actual event statistics with relative risk stats. i get the impression he should get some more life experience under his belt before he loses the plot altogether. He does not appear to be working in an HCP setting, and is doing academic medicine to earn a quick buck on the internet.(Edit to correct a typo - I meant quick not quack) just out of nappies and med school, and too busy polishing his MD credential, i suspect, He is not an expert yet.
Apologies. He is currently working as an EMT.
 
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Jaylee

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Did they have lasers in those days? I think that even now the photo's are not the prime diagnosis tool I had my scan last week, and the opthalmologist eyeballed me for some time before confirming diagnosis. I will need treatment some time, but not yet, and I am still able to drive. My problem is not diabetes related but is caused by a blocked cartoid artery following a stroke or two..

Seems the Doc is confusing actual event statistics with relative risk stats. i get the impression he should get some more life experience under his belt before he loses the plot altogether. He does not appear to be working in an HCP setting, and is doing academic medicine to earn a quick buck on the internet.(Edit to correct a typo - I meant quick not quack) just out of nappies and med school, and too busy polishing his MD credential, i suspect, He is not an expert yet.

Some of the scans in that era were in a mobile cabin in the car park of my surgery at that time?
They were "Poleroid" instant photos. Then clipped (stapled.) left & right respectively to the to the top of a patient form..
One guy doing the "photo shoot" was an older T1 himself. He couldn't stop bending my ear on "diet.?"

I learned a long time ago asking a photographer what any of this "stuff" means...
 

Jo_the_boat

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Type 2
Treatment type
Diet only
Seems the Doc is confusing actual event statistics with relative risk stats. i get the impression he should get some more life experience under his belt before he loses the plot altogether. He does not appear to be working in an HCP setting, and is doing academic medicine to earn a quick buck on the internet.(Edit to correct a typo - I meant quick not quack) just out of nappies and med school, and too busy polishing his MD credential, i suspect, He is not an expert yet.
Apologies. He is currently working as an EMT.

Yes, he's a young guy, can't possibly have lifetime experience. But that's why he seems to base his blogs on valid research and conduct his interviews, often with people with a lifetime's experience. (Malcolm Kendrick for example). The thing he is is young, he can't really help that, but being young he does have a vested interest in medium / long term trends both medically and lifestyle.
Much of the advice upon which the western world has based it's diet for the last 60 years is plain wrong, propagated still by middle-age, grey-suited people, many with vested interests, particularly financial. In fact, we're being pulled in a tangential direction too by the minority vegan / vegetarian brigade. Now, in my opinion, there's nothing wrong with following a vegan veggy lifestyle BUT, and I've had a few discussions with people about this, many don't realize that the foods they are eating in place of good meat for example are made of highly-processed alternatives. 'Alternative' burgers for example. Vegan, yes. Healthy, no.
You would have thought that our young doctor, dashing around the emergency room in his nappy, would be of a similar mind to the modern 'shouty' brigade, promoting 'new' thinking, such as veganism. But he doesn't actually. What he does is bring us (and that includes me who is past middle-aged) is fresh thinking. And I, as someone who should logically side with the grey-suit gang, find his research-based thoughts on such as saturated fat, low carb, vitamins, covid and exercise refreshing and informative.
The point is that he's adding to the public knowledgebase. He's not telling us what to do, just offering something we can listen to or not.
The other point is that if his views were wildly inaccurate or dangerous, people would definitely not listen or read his stuff. That would enhance neither his reputation nor bank balance.
 

Dark Horse

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1,840
I maybe wrong.. But diabetic scan eye checks back then for retinopathy (1998?) which is what the blog is talking about, were just a Poleroid pics taken of the back of the eye.. (Looked like fuzzy pictures of Mars to me..) Then the two images stapled to a patient form & pawed over & discussed by an eye doc.. No high def digital imaging emailed at that time..? Been doing this stuff for 46 years..
Yes, Polaroids were used in the early attempts at screening - useful but less sensitive than the digital imaging imaging used today. However, if anything suspicious had been seen on the Polaroid, that would have been followed up with a slit lamp examination to determine whether treatment was needed, just as it is today.
 

Oldvatr

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>>>>>>
The other point is that if his views were wildly inaccurate or dangerous, people would definitely not listen or read his stuff. That would enhance neither his reputation nor bank balance.
They listen to Trump and his cronies like Marjorie Taylor-Greene/ They listen to Fox News and Tucker Carlson. Doesn't seem to be detrimental to any of their bank balances. I find that bloggers and influencers on the net who are reliant on their outpur to fund themselves move towards entropy over time and gradually lose the plot. Be careful of the echo chamber effect. Just because he seems to be supportive of Low Carb WOE, so seems to agree with this website be mindful that none of us is perfect, and his inexperience and ideaology may lead astray. As @Dark Horse pointed out it is good to query things even where we agree.
 

Oldvatr

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I find paragrahphs in the OP that seem to be very simplistic and incorrect, such as
"Type 2 diabetes, on the other hand, is a lifestyle disease, caused by excessive consumption of refined carbohydrates. This results in metabolic dysfunction and “insulin resistance” (a state in which muscle cells and fat cells stop responding normally to insulin, which causes glucose levels to rise in the blood stream). While type 1 diabetics literally produce no insulin, type 2 diabetics produce plenty of insulin."
T2D is not a lifestyle disease, and it is not proven to be caused by refined carbs. There are other factors involved. Not all T2D have plenty of insulin

From other reviews of the UKPDS study there was consensus that the study demonstrated that intense intervention therapy for diabetes did not improve most of the outcomes such as stroke or heart attack, and had minial effect on retinopathy and neuropathy. The incidence of hypoglycemia was higher. Other research since that study have shown from meta analysis that intensive therapy can reduce life expectancy.

This is a more recent meta study
https://www.bmj.com/content/343/bmj.d4169.short

There is a study currently running to investigate intensive therapy in a T2D specific cohort
http://citeseerx.ist.psu.edu/viewdoc/download?doi=10.1.1.510.8487&rep=rep1&type=pdf
 
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