There are two diseases that share the name “diabetes mellitus”. This is unfortunate, because the diseases have very little in common, except for the fact that both are associated with high levels of glucose in the blood stream. Type 1 diabetes is an auto-immune disease, in which the immune system destroys the insulin producing cells that reside in the pancreas. Type 1 diabetics quickly die if they aren’t treated with insulin. For them, it is immediately and dramatically life saving.
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.
So, when a person with type 1 diabetes takes insulin, they are replacing a substance that they are lacking, and which they need to survive. When a person with type 2 diabetes takes insulin, they are taking more of a substance that they’re already producing a ton of. There is no immediate survival benefit.
So why would anyone ever come up with the idea of giving insulin to people with type 2 diabetes, who already produce lots of insulin?
That is a very reasonable question. Here’s a long-winded answer: Insulin is a hormone, i.e. a signalling molecule that circulates in the blood stream. Among its many functions is telling muscle cells and fat cells to hoover up glucose from the blood stream. Like I said before, the one thing type 1 and type 2 diabetes have in common is that the levels of glucose in the blood stream are high. In type 2 diabetes, the muscle cells and fat cells don’t respond normally to insulin, but they can be “bludgeoned” in to doing what they’re supposed to if they are given a sufficiently high dose. Which is why doctors frequently give insulin to type 2 diabetics.
The extra insulin helps to lower the blood sugar. But does that actually matter?
Well, that’s where it gets complicated. Blood sugar is a surrogate marker, just like blood pressure and LDL-cholesterol. What really matters to people is whether they have a decreased risk of bad outcomes, like strokes and heart attacks, not what their specific blood sugar level happens to be. It has been assumed that the harms associated with type 2 diabetes are primarily due to the high blood sugar levels. Which is a reasonable hypothesis, but it needs to be tested.
We don’t care about lowering blood sugar if there is no beneficial effect on survival, or heart disease risk, or risk of blindness, or something else that patients actually care about. Additionally, lowering blood sugar with insulin isn’t a harm-free intervention. First of all, insulin dosing is hard to get right, and it’s quite common for people taking insulin to accidentally overdose and end up experiencing an episode of hypoglycaemia (which can occassionally be fatal). Second, insulin raises blood pressure. Third, insulin makes you fat. So any potential positive effects that you get from insulin use need to be weighed against the negative effects.
Proponents of insulin treatment for type 2 diabetes usually point to the UKPDS study, which was published in the Lancet in 1998. Since it forms the basis for the opinion that it’s a good idea to give insulin to type 2 diabetics, it’s worth looking at in some detail. So, here’s what happened.
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 (which is quite low, actually within the range of what is considered a normal fasting blood sugar for a non-diabetic), or “relaxed” blood sugar control with diet, in which active measures with blood sugar lowering drugs were only taken if fasting blood sugar went above 15 mmol/l (a level that is high enough that it causes lots of doctors and nurses to panic).
In other words, the study was testing two quite extreme strategies, one in which blood sugar was lowered aggressively, and one in which nothing was done about blood sugar unless it went very high. The participants were followed for an average of ten years, which is a long time, and combined with the fact that there were almost 4,000 people in the study, this is definitely enough data to show a meaningful difference in outcomes if one exists. So, what happened?
Well, fasting glucose and HbA1c (a measure of average blood sugar over the last month or two) were significantly lower at all time points throughout the study in the intensive treatment group, so the insulin treatment was successfully keeping blood sugar levels down. But did this make a difference to any of the hard outcomes that people actually care about?
Let’s look at the hardest of hard outcomes first: death. 0.2% of participants in the insulin group had died after ten years. In the control group, 0.2% of participants had died. In other words, there was no difference in mortality.
Next, let’s look at heart attacks. 16.4% of participants in the insulin group had a heart attack, compared with 18.1% in the control group. That is a measly 1.7% reduction in risk over ten years. It wasn’t statistically significant.
Now, let’s look at strokes. 4.6% of participants in the insulin group had a stroke over ten years, compared with 5.2% in the control group. That is a 0.6% reduction in risk over ten years, and again, it wasn’t statistically significant.
What about outcomes that we worry about more specifically with type 2 diabetes, such as amputation?
Well, 1.9% of those treated with insulin experienced an amputation during the ten years, compared with 1.7% of those in the control group. Oops – There were slightly more amputations in the insulin treated group than in the control group.
So, why then are there doctors who think this study shows that it’s a good idea to give insulin to type 2 diabetics?
Well, it all comes down to one outcome – microvascular disease (the fancy name given to a set of diabetes complications that includes impaired vision, reduced sensation in the feet due to nerve damage, and loss of kidney function). 8.5% of participants in the insulin group suffered a microvascular complication, as compared with 11.6% of participants in the control group. In other words, the insulin treated group were 3% less likely to suffer microvascular complications after ten years.
That would mean that you could avoid a microvascular complication in one person for every 33 people treated with insulin for ten years. Which doesn’t feel like a very impressive effect to me, but the authors of the study spin this as a “25% reduced risk of microvascular complications” (yes, 8.5% is 25% less than 11.6%, when speaking in relative terms – read this if that makes no sense to you). It might be worth noting here that the study was part-funded by drug companies that make and sell insulin – not that that in any way influenced the authors of the study…
According to the authors of the study, the 3% (or “25%”, depending on how you choose to think about it) difference was statistically significant, but it wasn’t.
Warning – this next bit gets nerdy: The p-value for the difference was 0.015, which the authors consider statistically significant, because they’ve forgotten (as almost all medical researchers do), that the normal cut-off for statistical significance (p = 0.05) only applies when you’re looking at one endpoint. When you’re looking at 14 endpoints (as the authors of the study were), you’re supposed to correct for the fact that you’re looking at lots of relationships by dividing 0.05 by 14, which gives a p-value for statistical significance of 0.0036. The reason you have to make this correction is because, if you’re looking at lots of endpoints, then you’re going to get some that seem statistically significant just by chance, even though they’re not. Since 0.015 is more than 0.0036, the difference between the groups was in fact not statistically significant.
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). 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.
There was, in fact, no difference in visual acuity between the insulin treated group and the control group at ten years. Nor was there a difference in the proportion with absent ankle reflexes or knee reflexes between the groups (which is used as a sign of nerve damage in the lower extremities). So it’s highly questionable how meaningful the small reduction in “microvascular disease” was, even if it had been statistically significant (which it wasn’t).
So, the UKPDS study showed marginal reductions in heart attacks, strokes, and a questionable measure of microvascular disease among those treated with insulin after ten years of treatment, none of which was statistically significant. That is the entire basis on which millions of type 2 diabetics are currently being treated with insulin.
The rationale feels pretty weak to me, especially when you consider that there are downsides to insulin therapy – multiple daily injections, a need to monitor blood sugar continuously, weight gain, and an increased risk of hypoglycemia. In the UKPDS study, the annual risk of a serious hypoglycemic episode was 0.1% in the control group, but 2.3% in the group treated with insulin. That means that for every 45 type 2 diabetics treated with insulin for one year, one will suffer a serious episode of hypoglycemia (the definition of which is hypoglycemia so severe that it requires rescue by a third party or hospitalization). Note, that isn’t over ten years like all the previously discussed effects, that is over one year. And if we look at more minor episodes of hypoglycemia, 36.5% of participants in the insulin group suffered an episode of hypoglycemia per year of treatment (compared with 1.2% among those in the control group).
An even bigger trial was published in the New England Journal of Medicine in 2012. 12,537 people over the age of 50 with type 2 diabetes or pre-diabetes and cardiovascular risk factors were randomized to receive either long-acting insulin plus “standard care” or just standard care on its own. The goal was to see whether insulin would be useful as an adjunct in people who are at particularly high risk of cardiovascular disease. Among those getting insulin, the dose was raised until a target fasting glucose level of 5.3 mmol/l was reached. The participants were followed for an average of six years. So, what were the results?
Despite the fact that the insulin treated group managed to maintain lower blood glucose levels throughout the six year study period, there was no difference between the groups in terms of mortality, heart disease risk, stroke risk, amputation risk, or microvascular disease risk. Basically, six years of treatment with insulin provided no beneficial effect whatsoever, even though this was an older group at particularly high risk of cardiovascular complications (which should increase the odds of seeing a difference between the groups massively).
What can we conclude?
The evidence that exists really doesn’t support treating type 2 diabetics with insulin. It’s questionable if insulin provides any benefit whatsoever, and if it does, then the benefit is tiny and easily outweighed by the harms. As I’ve discussed previously on this blog, type 2 diabetes can be effectively treated with a carbohydrate restricted diet. In fact, a carbohydrate restricted diet is by far the most effective treatment in existence when it comes to type 2 diabetes, and can often reverse the disease completely. That is where physicians should focus their efforts.
I think the same can be said of the other type 2 medications. One of them (metformin) attacks your mitochondria, another one gets you to excrete sugars in urine (a bad sign normally) and god knows what the other one does.
Would love to see a post on this. I’m unconvinced that medication is the answer.
Got a reference for Metformin attacking the mitochondria?
The Internet book of Critical Care
https://emcrit.org/ibcc/metformin/
Very interesting, thank you.
Relative reduction – what a ‘con’.
Sounds like statins all over again!
I wish I had saved the original full page Lipitor ad which I distinctly recall from USA today featuring Jarvic ,which purported a 33% reduction in cardiac event as a headline with *
* “that means in a clinical study there were 2 events vs 3” or something to that effect …
Very interesting. I’m a T1 but I have been active in the past in mixed T1/T2 communities online. I’ve always thought giving insulin to T2s was a bad idea. You don’t mention that insulin doses to T2s rise inexorably and basically continue the spiral that gave them T2 in the first place.
As a T1 I do think microvascular complications are important and serious. And eye issues maybe most important. Can you dig in to that aspect a bit more? Are the other measures besides visual acuity? As an aside and anecdote, my vision has degraded constantly in real terms and yet I always get a perfect score for visual acuity. So whatever visual acuity is measuring, it is not what patients experience as “good eyesight” – mine is now terrible. Terrible yet “perfect”.
I can see one possible cause of bias on the eye data, which would be a higher propensity of clinicians to advise laser surgery when the patient presents with high long term blood sugar (HBA1C).
Definitely a supporter though I would have to check whether I’m a Patreon.
To expand on the ‘spiral’ for the benefit of readers:
A high carb diet causes high insulin levels
High insulin levels cause insulin resistance in cells
Continuing the high carb diet causes increased insulin production to overcome the insulin resistance
This in turn increases insulin resistance
The result of this spiral is: T2 diabetes
The observation of most T2s on insulin is that their insulin dose requirements increase inexorably over time. Doses in the hundreds of IU are not uncommon – these would be lethal doses to a T1 diabetic or a normal person.
So basically giving insulin to T2s is perpetuating and intensifying the exact disease mechanism that gave them T2 in the first place. Outside of acute situations, it seems madness to me to treat T2s with exogenous insulin.
There is a suggestion that the development of type 2 could be associated to sub clinical hypothyroidism. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3139205/
Thank you again, Dr Rushworth.
I wish the public health authorities, seize this great opportunity they now have to bring more attention and inform people how to live healthy lives.
Just like you are trying to do!
The window of oppurtunity is shrinking as the Covid-19 pandemic fades away and people will focus on the next crisis, whichever it may be.
People are smart enough to understand that a healthy lifestyle is helps more than pharmaceuticals but many need nudging and reminders since there are powerful forces working against this.
(For example, look at the current offers from your supermarket and you will see what crap.they try to push…)
Thank you for cutting through the nonsense that gets propagated.
Future historians will no doubt wonder how Big Pharma has been able in this era to be so effective in enlisting doctors, health authorities and governments as their sales force for so many dubious interventions.
That’ s the point. And we cannot be supprised……
Sorry:
…..surprised…..
P.V. Rasmussen
A low-carb diet, or actually fast for a week, which many claim will reverse the condition entirely?
I am glad you took up this. It shows one the first thing I tech to medical researches I help, e.g. to always be aware of the need to dived outcome P values by the number of outcomes you are looking at. Amazing that researches think that that was a significant result in the first study.
It should be multiply (typo by me) Sorry!
Thanks for another informative discussion. It saddens me that so many are ignorant of the fact that they are at risk of developing full T2 diabetes if they eat a typical western diet. As you say, the key is to cut out carbohydrates, particularly the refined ones that are so prevalent in modern processed foods. We are all at risk of developing insulin resistance, which is a slippery slope to a drug-supported existence until death from heart failure. The longer you leave it before going low-carb (and, more importantly, low on processed food) the harder it becomes to adjust. I’m in my late 60s and have done it over the last year but it’s taken time to settle down (and not lose too much weight!)
Your recent interview with David Unwin was inspiring but I don’t recall him mentioning his wife’s book: A fork in the road by Dr Jen Unwin. I found it really helpful.
Excellent analysis. 100% Rushworth!! I didn’t know the case for insulin therapy in type 2 diabetics is so weak.
Lots of stuff not very accurate here. You got type 1 right. Type 2 is not nearly so simple as you describe it. Insulin resistance is multifactorial, with genetic and acquired components, the latter having to do mostly with increased visceral fat. Insulin production, with is increased at first to compensate for the insulin resistance, later becomes disordered, with delayed post-prandial response and then progressive decline to subnormal levels.
A host of differing dietary prescriptions may be effective, but when they are so, are usually linked to the fundamental effect of decreasing visceral fat. Any diet which accomplishes this result usually brings improvement. But dietary measures alone are most definitely not usually sufficient to reverse diabetes, and there are numerous genetic and physiologic reasons for this situation.
There is much more to management of type 2 diabetes than control of hyperglycemia, but hyperglycemia is important nonetheless, both for prevention of microvascular complications as well as other metabolic and physiologic consequences. Reducing advanced microvascular disease in even a small number is critical for those who are affected. However, it’s also important to note that microvascular disease that may not be clinically evident is present in large numbers of those with diabetes as time goes on and that this situation certainly has an impact on the individual’s long term health outcome. And so, although a great many options exist today to control hyperglycemia in type 2 diabetes, insulin is still useful as an available choice, and particularly in the lesser frequency group of lean type 2 patients who generally have significant decreased beta cell function.
Have you seen the Newcastle studies?
Have not. Do you have a comment or reference?
This UK study also suggests that a low-carb approach can bring health benefits across the board. https://nutrition.bmj.com/content/early/2020/11/02/bmjnph-2020-000072
Here is a link to the Newcastle University studies by Prof Roy Taylor. The academic papers can be found off this link:
Hmm this web page comment form here won’t let me paste the link. Sorry. Search Prof Roy Taylor, Reversing Type 2 Diabetes.
I looked at the article. The problem is that the data for specific dietary prescriptions in diabetes 2 is conflicting. The proponents of low carb intake theorize that decrease in hyperinsulinemia has beneficial effect but in actual practice the studies like the one you mentioned aren’t very convincing if they don’t control for things like the effect of weight loss, etc, and often don’t follow patients long term. Clearly increased visceral fat is the major reversable component of insulin resistance and metabolic syndrome and my impression of the literature is that adherence to any diet that achieves this result is effective.
The other point I would make is that the idea of eliminating diabetes by diet is misleading since there are a host of genetic components waiting in the wings. You should look at the data for the impact of bariatric surgery on diabetes. In this case the procedures appear to have an impact on abnormal production of gut hormones like GLP1 in which case one can legitimately speak of some sort of reversal.
I think of diabetes as end stage hyperinsulinaemia. According to what I have read from the older research eg of Gerald Reaven, Joseph Kraft, John Yudkin, it seems to me that we should be looking for metabolic imbalances much earlier. Makes no sense to wait until the end stage – especially when the solution would be a simple dietary change. Apparently it takes 10 – 15 years for diabetes to appear, during which time insulin resistance is slowly increasing, with microvascular damage beginning about half way through, and presumably the other complications mentioned in Anthony’s post gradually accumulating as well. Joseph Kraft’s glucose challenge tests which plot the pattern of blood glucose over a few hours giving distinct patterns look like a good starting point for measuring pre diabetic hyperinsulinaemia or insulin resistance. I don’t think just monitoring blood glucose is enough. I also think we need to revisit our disastrous dietary guidelines.
I agree with Dr Perry re insulin levels in T2DM falling to subnormal levels over time. I have seen patients with T2 of 8-10 years duration present in diabetic coma as oral treatment failed. Obviously they now need insulin but I agree that insulin from the onset of diagnosis is wrong. Patients can end up being treated with massive amounts of insulin because high blood sugar levels are seen and treated as insulin resistance. I believe they are suffering from unrecognised hypoglycaemia between tests resulting in diurnal reactive hyperglycaemia similar to the overnight effect described by Somogyi. These patients end up living a miserable existence while experiencing hypo upon hypo as their insulin dose is mistakenly ramped up
Dr Rushworth
To what extent is insuline given to T2 patients in Sweden, nowdays?
Really well done Sebastian. Depressing . Sometimes the facts do that.
Hi Sebastián, thanx again. You are right, low carb diet, preferably including other pillars of a better lifestyle, help improve and sometimes even reverse DM2 quite impressively. As does caloric restriction.
I did however see a diabetic that showed no benefit of a low carb diet, on the contrary: she got sicker. She needed insulin at first in the hopes of progressing to low carb later. And indeed, she lost weight while taking insulin and her HbA1C improved.
And: sometimes it’s stress that causes the DM2 or even medication like topical corticosteroids that cause weight gaining and from there progresses to DM2.
Thanks again for another great article.
Very interested to read about the low carb diet, and also how it can impact not only diabetes, but also hypertension.
Could you possibly do an article on hypertension at some future point?
Or indeed, have you already addressed this?
Best regards, Kristy
‘Ron’ has been a type 2 diabetic since approx 1998. He is now approx 82 yrs old. He has had 3 cataracts removed and is now being told there are signs of impaired vision problems in the retina.
He was once very fortunately found in time, unconscious, due to Hypoglycaemia. But that was following an unusual alcohol binge (rum) the night before!
Before he was diagnosed, he did take sugar in his tea but apart from that so far as I know his diet was not bad. He was a bit fat around the waist though clearly well muscled in chest and limbs. So nothing unusual for a man of that age, with that body shape.
I have become very sceptical about pharmaceutical interventions in general and the U.K. N.H.S. – or perhaps all countries’ health services!
I do not know exactly what he is taking for what but it does seem to me that he is being treated for far more than just high blood sugar levels.
Why? Does type 2 diabetes make him more at danger from high blood pressure or LDL cholesterol? Does he need to be on drugs for high blood pressure or statins to lower cholesterol.?
‘They’ have twice pressured me to take statins! The second time the admission eventually came out – ‘for statistical reasons’!
I have come to the conclusion that we would do better to stop interfering so much with the innate immune system at the behest of the pharmaceutical industry.
Absolutely, agreed.
Thank you Kristy.
Don’t know about you but I wish I could do more about it.
Somehow, wake everybody up to what is going on and persuade them to question things more.
Medical science has made tremendous progress in the last century but their is no excuse for ‘their’ arrogant assumption ‘they’ can do whatever they choose with OUR bodies (or minds).
Interesting, thank you for your work!
Have you heard of anyone with diabetes type 1 that managed to get cured, or at least got some insulin production going?
I have heard of people with other auto immune disease that has been cured with a very strict diet, and was thinking that if we manage to find out what triggers the immune system to attack the insulin producing cells, mabe even type 1 can be cured..
Good stuff, Dr Rushworth; thank you. Now a question: we’ve found an old newspaper cutting describing an experiment comparing the eating of pasta in the usual way, and eating it after it has been allowed to cool and is then reheated. The claim is that the second method causes less of a spike in blood sugar.
Do you happen to know of any work on this topic?
My son in law has severe hereditary gout since his teens. He also has TII diabetes. The doctor arranged for dietitians to advise him. The dietitian he was sent to for gout recommended low fat/high carbs. The diabetes dietitian recommended low fat/high protein from beans (high in purines). In fact he needs to get his protein as much as possible from eggs and milk products (low purines) and at least 60% of calories from fat.
Dieticians are about as much use as epidemiological modellers. Perhaps I exaggerate a little but probably not much.
dearieme.
Epidemiological modelers – you mean like Ferguson and SAGE, here in the U.K.?
Far from exaggerating you have grossly understated the harm they do!
Over many years they have warned ‘Be afraid be very afraid, you are all going to die unless you cull x million animals, or . .x . .y . .z ‘.
The latest of course being – give up ALL your democratic rights and freedoms, be locked into your own home and don’t go to work, etc..
At least Sebastian spoke out about the Covid Scam! (Amongst others.)
Not having either gout or type 2 diabetes I can not comment personally on dieticians advice on those. But I certainly agree with a previous post about advice on losing weight. Far from eating a high carbohydrate low fat diet anyone needing to lose weight will do better to eat a high protein diet. Don’t worry about fat. Just count the Carbs keeping them low.
Personally I have come to the conclusion that our N.H.S. here is Run by Global Pharma and our Leaders listen to ‘experts’ who, like themselves, work for U.N. Agenda 21.
I am not a doctor, but I own a body!
When I was diagnosed with gout, I went to the internet as anyone with any sense does does nowadays, and was advised to drink more water. The idea was that this would help to disolve the crystals of uric acid that form in the joints. I found that cleared my problem over a period of a few days.
Doctors should obviously suggest this as a first line of attack, but clearly don’t.
Mainstream dieticians are a disaster, actively harmful. They regurgitate dogma that has no evidence base, like it’s religion, and have no understanding of biology. They are hacks.
However there are some very good alternative nutritionists.
Spike. Alternative nutritionists, sounds good to me!
Sounds a bit like the ‘wise women’, back in medieval times! They did far less harm than the ‘physicians’ of that time.
Us peasants have had the chance of more education nowadays. Hopefully we have not been completely brainwashed out of our common sense. That should lead us to think for ourselves and look after ourselves!
Antibodies wane after Covid infection as well as after Covid vaccination, and health authorities recommend boosters to keep the levels high “in case there new variants come”. Is there any risk for the individual with permanent high levels of antibodies?
Marc Girardot argues that during an infection a temporary disbalance is an acceptable tradeoff to fight the virus: high fever, temporary invasion of T-cells and antibodies. Evolution, Girardot continues has chosen a path of dissipated fever, suicidal T-cells and slowly reduced antibodies, because too long a fever would break down healthy cells, and perpetual specialised T-cells can attack healthy cells and “very high levels of antibodies with nowhere to go are also extremely dangerous. They can passively bind to receptors of healthy cells, and kickstart a cascade of autoimmune diseases”.
Girardot’s argument sounds compelling but I would like to see sources that support it.
Source: “No one would ever accept permanent fever… So, why accept permanently high antibodies? It’s a “Death Zone”!” Marc Girardot, jan 30, 2022
For those who want to understand the reasons behind the results provided in the above article, I suggest the definitive book:
Dr. Jason Fung – The Diabetes Code.
https://www.amazon.com/Diabetes-Code-Prevent-Reverse-Naturally/dp/1771642653/ref=tmm_pap_swatch_0?_encoding=UTF8&qid=1645662461&sr=8-1
I wonder if chromium deficiency might account for some insulin resistance and type 2 diabetes.