Currently around 1 in 16 people in the UK suffer from diabetes with this ratio equating to a total of around 3.9 million people; these figures alone provide cause for concern. Our article this week is provided by Dr David Morris – a freelance General Practitioner in the NHS and a recent speaker at one of our Cytoplan seminars.
In the article below Dr Morris looks at how one of the fundamental problems with much of modern medicine’s approach to health is it’s constant failure to go back to basics and genuinely understand the first principles of the roots of health and illness; a clear example of this being the treatment of Type II Diabetes, where much of modern medicine targets lowering blood sugar without ever targeting the problem of insulin resistance.
One of the fundamental problems with much of modern medicine’s approach to health is the failure to go back to basics and genuinely understand the first principles of the roots of health and illness.
Nowhere is this more apparent than in the management of Type II Diabetes. Given the literally millions with this condition and the many millions more heading towards this condition with so-called “pre- diabetes” then this of incredible concern.
In this blog post I will set the scene explaining the issue of insulin resistance and in the next post explain how insulin resistance can be treated.
What is the concern at the heart of the management of Type II Diabetes?
It is as simple as this; doctors and patient’s alike know that running high blood sugars is bad for you – the excess sugar sticks to your cell proteins distorting and damaging them – try using your smart phone with candyfloss all over your fingers – the sticky sugar doesn’t exactly help!
BUT while doctors know that Type II diabetes is caused by insulin resistance – which leads to elevated insulin levels (alongside elevated blood glucose) – there appears to be an almost complete failure to understand that raised insulin is MORE harmful than raised blood sugar.
As a consequence all of the effort is targeted at lowering blood sugar without ever considering the elevated insulin and targeting insulin resistance.
Even worse – many of modern medicine’s approaches to lowering blood sugars actually worsen insulin resistance which leads to even higher levels of insulin with even more harm from this.
Research confirms that the outcomes from the current approaches to treating Type II Diabetes in this way is definitely failing:
1.If you have Type II Diabetes but you do not yet have symptoms then you are no better off being screened and having the diabetes treated –
It seems common sense that we should screen people for diabetes before they have symptoms so that they don’t end up with damage before they are diagnosed.
Unfortunately a large trial (1) screening thousands of people for diabetes showed that overall they did not do any better than people that were not screened.
Diabetes was identified successfully but the approach to treating it appears to be unhelpful –in fact the screened group had a higher death rate then the unscreened group. Although this was not “statistically” significant it is the opposite of what we expect.
2. If you use conventional approaches to achieve very good (tight)lowering of blood sugar then in fact you are more likely to come to harm and die-
In a large trial (2) of more than 10,000 patients the participants were randomised to intensive versus normal treatment i.e. “ok” sugar control versus “very good” sugar control.
The trial had to be halted after 3.5 years because “As compared with standard therapy, the use of intensive therapy to target normal glycated haemoglobin levels for 3.5 years increased mortality and did not significantly reduce major cardiovascular events.”
3. Using insulins to treat Type II Diabetes increases the death rate.
The use of insulin to treat Type II Diabetes in the UK has increased by 750 per cent over the last 20 years but the question is rarely asked whether it helps or not.
A large trial (3) of 84, 622 primary care patients measured the risk of first major adverse cardiac event, first cancer or death. It concluded that – “exogenous insulin therapy was associated with an increased risk of diabetes-related complications, cancer, and all-cause mortality”
So we can conclude from this that all is not well in the world of conventional diabetes treatment – to understate the issue!!
We MUST instead seek instead to understand the mechanism for developing Type II Diabetes and address this issue NOT simply address the consequence of raised blood sugar – of course if we do this then the raised blood sugar will resolve too.
Returning to basics
What does insulin do?
It is clear that one of the roles of insulin is to lower your blood sugar – it “pushes” glucose inside your cells out of the blood stream and prevents the production of new glucose by the liver.
BUT this is only one of many, many roles of insulin…
Insulin and LIPID metabolism:
- Increases lipid synthesis – insulin forces fat (adipose) cells to take in blood lipids/fats.
- Increases esterification of fatty acids – forces adipose tissue to make and store fat.
- Decreases lipolysis – reduces conversion of fat cell lipid stores into blood fatty acids (which can be burned as fuel.)
- Prevents breakdown of fat into ketones which are another important fuel source especially for the brain.
i.e. insulin MAKES YOU FAT!
Insulin and Protein metabolism:
- Decreases proteolysis – decreasing the breakdown of protein.
- Increases uptake of amino acids into cells to make protein.
i.e. insulin promotes muscle growth
Insulin and Detoxification:
- Decreases autophagy (programmed cell death of damaged/aged cells) and toxin removal- leads to less degradation of damaged cells.
Insulin and Atherosclerosis:
- Directly triggers atherosclerosis – infusion of insulin into a carotid artery triggers atherosclerosis in that artery but not the contralateral artery.
Insulin and Magnesium:
- Promotes the movement of magnesium inside cells which is one of the most vital minerals in our body.
Insulin and Sex Hormones:
In men, insulin speeds up the action of the enzyme aromatase which increases the conversion of testosterone to oestrogen- not a good thing particularly as raised oestrogen levels appear to promote metabolic syndrome.
In women, high insulin speeds up an enzyme called 17,20-lyase, and this increases the production of testosterone leading to Polycystic Ovarian Syndrome- the number one cause of infertility.
Understanding Insulin Resistance
When receptors are constantly exposed to high levels of insulin they down regulate and THEY BECOME RESISTANT TO INSULIN.
A way to understand this is to think of the experience when you are in a room when someone is vacuuming – your ears adjust to the noise and screen it out – and then you suddenly notice it has gone quiet when the vacuum is switched off.
The consequence of this lack of response leads to a vicious cycle as your blood glucose rises then…. then insulin levels rise further leading to more stimulation and then more resistance etc, etc
So if we put ourselves in a situation where our cells are constantly exposed to insulin eventually we trigger this vicious cycle of rising insulin BUT the consequences of this are more complex than we might think.
There are three problems that arise:
- The failure of a cell to respond to insulin.
- The different rates at which different organs/cell types become resistant to insulin – this means that some organs are overstimulated by the high insulin levels, alongside other organs being resistant and hence under stimulated by insulin.
- The need to metabolise/breakdown the high levels of insulin.
Failure to respond to insulin ie resistance
The most obvious consequence of this is rising blood sugars – insulin is unable not only to push glucose into cells (potentially starving them of an important energy source) but also cannot stop the liver from making new glucose and releasing it into the blood stream – hence we have raised blood sugar even on waking after overnight fasting.
A further consequence is that insulin is unable to push magnesium into cells- magnesium is vital for the production of energy in our cells and lack of magnesium leads to cellular fatigue. Magnesium is also required for muscle relaxation and so insulin resistant muscle cells do not relax fully.
While we might think of muscles as biceps and quads etc. of more significance is the muscle layer around all of our arteries – lack of relaxation of this leads to raised blood pressure with all of its potential consequences.
The problem with differential rates of organs development of insulin resistance.
Having taken a snapshot of some of the many actions of insulin and understood why the failure to respond to insulin leads to harm, we also need to consider the impact of overstimulation due to high insulin levels because resistance does not develop equally in all cell types.
Roughly speaking it appears that organs develop resistance to insulin in this order:
Pancreas, Brain, Liver, Muscles then finally Adipose (fat) tissue.
It is not even as straight forward as this, as some cellular functions never become resistant to insulin and so this leads to constant over stimulation if insulin levels are high.
The pancreas obviously secretes insulin (from beta cells in the islets of Langerhans) but also secretes the hormone glucagon. Glucagon essentially does the opposite of insulin with respect to sugar- it makes your liver produce more glucose amongst other actions.
Insulin and glucagon in part inhibit each other’s release –if your body needs to lower blood glucose it makes sense to lower the production of the hormone that raises it. BUT with chronically high levels of insulin, the cells that produce glucagon (alpha cells in the islets of Langerhans) become resistant to the insulin signal and start to release glucagon despite high levels of blood glucose. Clearly this is the last thing that you require as this now contributes to even higher levels of circulating glucose.
The brain is particularly vulnerable to any problems with sugar metabolism because it consumes disproportionate levels of glucose and oxygen – it is 2% of body weight but uses 20% of the body’s glucose and oxygen.
Evidence show us that people with dementia develop problems with the uptake of glucose in the memory parts of the brain up to 20 years before developing Alzheimer’s Disease (4) and also shows us that patients with advanced AD show higher blood but lower cerebrospinal fluid insulin (5) -this correlates with the dementia severity and indicates that the brain is no longer taking in insulin i.e. it has become insulin resistant.
Insulin secreted by the pancreas first passes through the liver so it is most exposed to high levels.
Once your liver is resistant to the insulin signal it will continue to make new glucose and also breakdown glycogen stores to release more glucose despite blood levels being high. You can see how the vicious downward spiral is further triggered.
Muscle develops resistance after the liver and this leads to poor uptake of glucose and reduced glycogen (glucose storage) formation in muscles. It also leads to muscle wasting due to lack of amino acid uptake to make protein.
Magnesium intake is also reduced alongside reduced glucose uptake so exercise ability rapidly plummets – the low energy and wasting leads to less exercise leading to more insulin resistance!
Adipose (Fat) Tissue
Eventually adipose tissue becomes resistant to insulin but up until that point there is a continuous insulin driven drive to lay down more fat. While people do not get fatter and fatter indefinitely the stimulation on fat cells by insulin continues long after other cell types have become resistant.
Blood Vessel Lining (Endothelial cells)
Endothelial tissue never becomes resistant to insulin. The ongoing rise in intracellular glucose leads to very high levels of damaged proteins (Advanced Glycaemic End Products AGE’s). This means that elevated insulin leads to continuously high levels of inflammation and atherosclerosis
There is a specialised protein called FOXO that acts by regulating the levels of other cellular proteins that are responsible for cleaning up cellular garbage. The action of FOXO is inhibited by insulin BUT insulin regulation of FOXO is completely normal in muscle in pre-diabetes and diabetes individuals – i.e. FOXO does not become insulin resistant.
In healthy individuals, insulin levels are only elevated for a short time each day, leaving FOXO active to clear garbage from the cell the rest of the time. If insulin levels are constantly high then the detoxification pathways remain persistently switched off.
The need to metabolise/breakdown the high levels of insulin.
Alongside the issues of all the signalling effects of insulin on cells, your body also has to breakdown the high levels of insulin.
This is a particular problem in the brain because the hallmark of AD is the development of beta-amyloid plaques. Insulin Degrading Enzyme (IDE) degrades insulin and beta-amyloid BUT preferentially degrades insulin.
So higher levels of insulin lead to less breakdown of beta-amyloid AND as a further complication Beta-amyloid will bind to insulin receptors -so high Beta-amyloid levels worsen insulin resistance!
What do current conventional medical approaches offer?
Dietary advice– eating lots of complex carbohydrates is still the mainstream advice – unfortunately this promotes higher levels of insulin and so is the last thing required. (More to follow in the next posting.)
This is actually helpful but not necessarily targeted in the most effective way. (Again more to follow.)
There have been a huge number of concerns with the safety of many of the drugs used to treat diabetes -while they all reduce blood sugar, they have other risk such as pancreatitis, heart failure, bladder cancer and a number have been withdrawn from use.
More pertinently, with the exception of metformin, they all act at least in part by elevating insulin levels so aggravate insulin resistance. You can see for yourself why using insulin injections directly shows such poor outcomes in Type II Diabetes.
Metformin does reduce insulin resistance but also inhibits the absorption of B Vitamins and raises the risk of heart failure so there are better options than this. (More to follow…)
In summary persistently raised insulin:
- Promotes obesity
- Disrupts the counteracting hormones i.e. glucagon
- Reduces cellular detoxification generally with numerous consequences
- Disrupts sex hormones
- Increases the risk of dementia
- Increases the risk of high blood pressure
- Increases the risk of atherosclerosis hence increases risk of heart disease, strokes and peripheral vascular disease
So if we fail to address insulin resistance but merely focus on lowering blood glucose it is clearly predictable that the outcome will be less than ideal.
David qualified as a doctor in 1994 and spent six years in hospital medicine – mostly in general adult medicine, but also in paediatrics and Accident and Emergency.
In 2000 David moved into family general practice and was a GP partner for many years. During this time he was also extensively involved in commissioning health care services. David also has significant training and experience in complementary therapies such as acupuncture and homeopathy, and ran a primary care based pain clinic for over a decade using acupuncture therapies. Dr Morris is a regular blogger – you can read more of his articles here.
With many thanks to Dr David Morris for this article. If you have any questions regarding the health topics that have been raised, or any other health matters please do contact me (Amanda) by phone or email at any time.
firstname.lastname@example.org, 01684 310099
Amanda Williams and the Cytoplan Editorial Team: Joseph Forsyth, Simon Holdcroft and Clare Daley
References are available upon request.
Last updated on 2nd February 2016 by cytoffice