The Tip of the Iceberg – the much bigger problem of high insulin levels

The US and Canada and much of the westernized world is in the midst of a Diabetes epidemic but this is just the tip of the iceberg when it comes the underlying metabolic disruption caused by insulin. The part of the iceberg that is visible and that people know about is hyperglycemia (elevated blood sugar) but the part that is invisible and that few are aware of  hyperinsulinemia (elevated blood insulin levels) which often precedes a diagnosis of pre-diabetes or Type 2 Diabetes by decades. It is this high circulating level of insulin that contributes to the significant risk of developing cardiovascular disease including heart attack and stroke, hypertension (high blood pressure), elevated cholesterol and triglycerides, non-alcoholic fatty liver (NAFLD), Poly Cystic Ovarian Syndrome (PCOS), Alzheimer’s disease and other forms of dementia, as well as certain forms of cancer including breast and colon / bowel cancer.

High blood sugar may or may not be a symptom of high levels of insulin levels and in the early stages of metabolic dysfunction almost 75% of people will have normal fasting blood glucose yet have abnormally high levels of circulating insulin.  As a result, these people are at increased risk of the metabolic diseases mentioned above but unlike someone already diagnosed with Type 2 Diabetes they have no idea!

High circulating levels of insulin is entirely missed by most routine lab tests because blood sugar is being monitored as the first indication that someone is becoming insulin resistant.  By the time blood glucose levels are abnormal, the β-cells of the pancreas that produce insulin are already being over-taxed to the point of exhaustion.  Physicians have “answers” (lab test results) but oftentimes are asking the wrong questions. That is, having normal fasting blood sugar or even HbA1C (3-month blood sugar average) does not necessarily mean everything is “fine”.  Most sobering is that by the time a person is diagnosed with Type 2 Diabetes they have already lost ~ 40% of their beta-cells mass sometimes more – cell loss which is currently thought to be unrecoverable.

The healthy human body maintains blood sugar in a tightly-regulated range between 60-100 mg/dl (3.3-5.5 mmol/L).  When a healthy person eats food containing carbohydrate – whether as the starch in bread, pasta and rice, the sugar in milk (lactose), fruit (fructose), simple table sugar (sucrose) or high fructose corn syrup in commercially prepared foods, special glucose-sensing cells in the small intestine release signalling hormones called incretin hormones in response to the presence of these carbohydrates. The incretin hormones tell the pancreas to release insulin which in turn tells the body’s cells what to do with the energy from the food we eat; either (1) burn it or (2) send it to the liver to store it, first as glycogen, and the remainder as fat (adipose tissue).  This is called fuel partitioning. When metabolic processes respond appropriately, blood sugar rises modestly after eating carbohydrate-based food but is quickly restored to its normal, tightly-regulated range soon afterwards.

Metabolic problems begin because people eat foods that contain some form of carbohydrate every few hours which results in frequent release of insulin. Glycogen levels in the muscle and liver remain close to full due to the steady supply of refined or processed carbohydrate-based food compounded by the reality that body’s cells are rarely challenged to use stored energy. In the early stages cells simply stop responding appropriately to insulin’s signal. This is called insulin resistance. Insulin resistance is the decreased ability of our cells to partition fuel. It can be compared to someone hearing a noise such as their neighbour playing music, but after a while their brain “tunes out” the noise.  Even if the neighbour gradually turns up the volume of the music, the person’s brain compensates by further tuning out the increased noise. To compensate for insulin resistance, the β-cells of the pancreas begin producing and releasing more insulin, which results in hyperinsulinemia – too much insulin in the blood.

In the early stages the body is simply trying to keep blood sugar levels within its normally tightly regulated range by making and releasing more insulin to force the cells of the body to take up the excess glucose and burn it, but this just makes the problem worse. It is the increasingly high circulating levels of insulin that contribute to the health risks and metabolic disease listed above.

Just as high blood sugar is not necessarily associated with high circulating levels of insulin, neither is obesity.  Approximately 1/3 of insulin-resistant people are lean. A person who is obese simply makes more fat cells (adipocytes) in order to store the excess energy as sub-cutaneous fat (fat under the skin) which serves as a protective mechanism. Contrary to what most people assume, people don’t become insulin resistant because they are fat; becoming fat may be a protective response to high levels of circulating insulin. Those who are lean but insulin-resistant are thought to have a lower ‘personal fat threshold’ than those that become overweight of obese. That is, they are limited in terms of how many new fat cells their body can make to store excess energy, so they store the excess energy in and around their organs in what’s called visceral fat.  This is where the metabolic disruption occurs.  Whether the person is obese or lean, once they have exceeded their personal fat threshold, the result is the same.

Assessing whether my clients have higher than ideal levels of insulin is as important as assessing whether they already have higher than ideal levels of blood sugar, in fact it is even more important. When people already have pre-diabetes or Type 2 Diabetes, they’ve likely been told by their doctors that they are increased cardiovascular risk and that this is a risk factor for other metabolically related conditions, including high blood pressure, fatty liver disease, Alzheimer’s and other forms of dementia and certain types of cancer. Having normal blood sugar many are told “everything is fine” when very often it is not.  These people are at risk and don’t even know it.

It is important that my clients know whether they have symptoms of hyperinsulinemia and to help them understand the factors that contribute to it. This helps people to have the motivation to make necessary dietary and lifestyle changes to reduce their disease risk and totally avoid the progression to Type 2 Diabetes, long before blood sugar levels begin to rise.

For those that already are pre-diabetic or been diagnosed as having Type 2 Diabetes, it is not too late. A carbohydrate-modified diet as well implementing very specific lifestyle changes makes the reversal of symptoms entirely possible and does not require dietary or exercise extremes.

I think that for too long we as clinicians have tackled this as an insulin problem caused by overweight and created by “eating too much and moving too little” rather than as the exact opposite; that people get overweight because of an underlying insulin problem. When we address hyperinsulinemia, weight, blood sugar, blood pressure and high cholesterol and triglycerides are corrected. There are studies documenting this (covered in previous articles) and my “A Dietitian’s Journey” tells my own sample-set-of-one story reversing Type 2 Diabetes that I had for 10 years, as well as the related conditions of high blood pressure and abnormal cholesterol and triglycerides. It can be done.

Have questions as to how I can help you either in-person in my office or via Distance Consultation? Please send me a note using the Contact Me form above and I will reply as soon as I am able.

To our good health!

Joy

 

you can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

Reaven, G., Insulin resistance, type 2 diabetes mellitus, and cardiovascular disease: the end of the beginning. Circulation, 2005. 112(20): p. 3030-2.

Reaven, G.M., Pathophysiology of insulin resistance in human disease. Physiol Rev, 1995. 75(3): p. 473-86.

Taylor, R. and R.R. Holman, Normal weight individuals who develop type 2 diabetes: the personal fat threshold. Clin Sci (Lond), 2015. 128(7): p. 405-10.

Reaven, G., The metabolic syndrome or the insulin resistance syndrome? Different names, different concepts, and different goals. Endocrinol Metab Clin North Am, 2004. 33(2): p. 283-303.

Crofts, C., et al., Identifying hyperinsulinaemia in the absence of impaired glucose tolerance: An examination of the Kraft database. Diabetes Res Clin Pract, 2016. 118: p. 50-7.

Ludwig, D.S. and M.I. Friedman, Increasing adiposity: consequence or cause of overeating? JAMA, 2014. 311(21): p. 2167-8.

Crofts, C., Understanding and Diagnosing Hyperinsulinemia. 2015, AUT University: Auckland, New Zealand. p. 205.

Copyright ©2018 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.)

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Part 2: How is Insulin Resistance Measured?

The introduction to this article (Part 1: What is Insulin Resistance)  explains what insulin resistance is, the conventional treatment for it and the drawbacks to that treatment: https://www.lchf-rd.com/2017/07/26/what-is-insulin-resistance/

INTRO: There are a number of tools available for measuring insulin resistance, most of which are more suited to a research setting, including the Quantitative Insulin Sensitivity Check Index (QUICKI) and the Matsuda Index.  Others, such as the McAuley -, Belfiore -, Cederholm -, Avignon – and Stumvoll Index are better suited for epidemiological (population) research studies and are often compared to the “gold standard” for the measurement of insulin sensitivity, the Hyperinsulinemic Euglycemic Clamp (HEC).

The homeostasis model assessment (HOMA-IR) method is suitable for individuals to use with their doctors or Dietitians to assess insulin resistance, and is useful for using over time to measure the impact of dietary and lifestyle changes in lowering insulin resistance.


Visualizing Insulin Resistance

Insulin resistance can be determined by measuring insulin response to a standard glucose load over a 5 hour period and plotting the Insulin Response curves – which is precisely what Dr. Joseph R. Kraft MD, who was Chairman of the Department of Clinical Pathology and Nuclear Medicine, St. Joseph Hospital, Chicago, until his retirement.

Dr. Kraft spent more than a quarter century devoted to the study of glucose metabolism and blood insulin levels – collecting data in almost 15,000 people, aged 3 to 90 years old. Between 1972 and 1998, Dr. Kraft measured the Insulin Response and data from 10,829 of these subjects indicated that 75% of subjects were insulin resistant.

Compiling this data, five distinct Insulin Response Patterns emerged.

Pattern I

The light green curve below, is what a normal insulin response should look like. Insulin levels should rise steadily in the first 45 minutes (in response to the standard glucose load) to no higher than ~60 mIU/L (430.5 pmol/L) and then decrease steadily until baseline by 3 hours.

PATTERN II

People who are in the early stages of insulin resistance (Pattern II, represented by the yellow curve) release considerably more insulin in response to the exact same glucose load. Insulin levels rise to ~ 115 mIU/L (825 pmol/L) in the first hour and then take considerably longer (5 hrs) to drop back down to baseline, than the normal response.

PATTERN III

People who have progressed in insulin resistance to Pattern III have insulin levels that keep rising for the first 2 hours and then drop off more sharply, back down to baseline.

PATTERN IV

Those with Type 2 Diabetes / very high insulin resistance (Pattern IV) release huge amounts of insulin almost immediately, reaching levels of ~ 150 mIU/L (1076 pmol/L) at 1 hour.  Then for the next 2 hours, insulin continues to climb, before it begins to decline to baseline.  Even at 5 hours, insulin levels never decrease to normal values.

PATTERN V

Is what is seen in Type I Diabetes (T1D), when there is insufficient insulin production.

Please see Significance of Insulin Resistance for more details on Dr. Kraft's findings: https://www.lchf-rd.com/2017/03/22/featured-significance-of-insulin-resistance/

While a 5 hour glucose tolerance test is not available at most labs, a 2 hour glucose tolerance test (2hrGTT) will indicate whether or not a person is insulin resistant or Type 2 Diabetic. 

However, once a person is already diagnosed as Type 2 Diabetic, most medical plans will not cover the cost of having the test re-performed in order to determine if insulin response has changed in response to diet and lifestyle changes.

This is where the the homeostasis model assessment of insulin resistance (HOMA-IR) comes in – a tool easily used by clinicians and relying on standard blood tests.

Homeostasis model assessment of insulin resistance (HOMA1-IR) – Matthew’s Equations (1985)

The homeostasis model assessment was first developed in 1985 by David Matthews et al and is method used which quantifies insulin resistance and β-cell function of the pancreas from fasting blood glucose and either fasting insulin or C-peptide concentrations.

Pancreatic β-cells are responsible for insulin secretion in response to increasing glucose concentrations, so when there is decreased function of the pancreas’ β-cells, there will be a reduced response of β-cell to glucose-stimulated insulin secretion.

In addition, glucose concentrations are regulated by insulin-mediated glucose production in the liver, so insulin resistance is reflected by reduced suppression of hepatic glucose production, stemming from the effect of insulin.

The HOMA-IR model describes this glucose-insulin homeostasis using a simple equation, based on fasting blood glucose and fasting insulin. The equation uses the product of fasting plasma insulin (FPI) x fasting plasma glucose (FPI), divided by a constant of 22.5, providing an index of hepatic insulin resistance:

HOMA1-IR = FPI (mu/I) x FBG (mmol/L) / 22.5

The “Blood Code” book is based on these 1985 equations. The problem with the Matthew’s Equations is that they underestimate Insulin Sensitivity (%S) and overestimate % β-cell function.

Homeostasis model assessment of insulin resistance (HOMA2-IR)

Oxford University, Centre for Diabetes, Endocrinology and Metabolism in the UK, has designed a HOMA2-IR model (2013) that estimates β-cell function (%B) and insulin sensitivity (%S) for an individual from simultaneously measured fasting plasma glucose (FPG) and fasting plasma insulin (FPI) values. It also can be used with fasting specific insulin or C-peptide values, instead of fasting RIA insulin.

The HOMA2-IR calculator provides % β-cell function (% B ) and % Insulin Sensitivity (%S): https://www.dtu.ox.ac.uk/homacalculator/download.php.

It is important to note that HOMA-IR values vary by ethnic group, but looking at humans as one, a normal HOMA-IR value for a healthy person ranges from 0.5-1.4

  • Less than 1.0 means you are insulin-sensitive which is optimal.
  • Above 1.9 indicates early insulin resistance.
  • Above 2.9 indicates significant insulin resistance.

Use of Tools

While these tools are primarily used by clinicians, knowing about them is useful in being proactive in managing one’s own health.  For example, if you have already started making the dietary and lifestyle changes to lower insulin resistance, having your fasting insulin measured along with your fasting blood glucose, will enable your doctor or myself to calculate your progress, as well as recommend adjustments in your plan.

Have questions?

Why not send me a note using the “Contact Us” form at the top of this web page.

To our good health!

Joy

you can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

References

Gutch, M, Kumar, S, Razi, SM, et al,  Assessment of Insulin Sensitivity / Resistance, Indian J Endocrinol Metab. 2015 Jan-Feb; 19(1): 160–164.

HOMA Calculator©, University of Oxford, Diabetes Trials Unit, Oxford Centre for Diabetes, Endocrinology and Metabolism: https://www.dtu.ox.ac.uk/homacalculator/download.php


 https://twitter.com/joykiddieRD

  https://www.facebook.com/lchfRD/


Note: Everyone's results following a LCHF lifestyle will differ as there is no one-size-fits-all approach and everybody's nutritional needs and health status is different. If you want to adopt this kind of lifestyle, please discuss it with your doctor, first.

Copyright ©2017 The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.

Part 1: What is Insulin Resistance?

The hormone insulin plays a number of roles, one of which is to help move the glucose that is produced from the digestion of food – from the blood and into the cells for energy. Insulin resistance is where the body isn’t responding to insulin’s signals to take up glucose, so blood glucose remains high, despite normal or high levels of insulin.

Type 2 Diabetes (T2D) is essentially a state of very high insulin resistance.

Insulin normally goes up when we eat foods that contain carbohydrate (breads, pasta, rice, fruit, milk products, etc.) and acts on the liver to help store the incoming food energy – first as glycogen and when liver and muscle glycogen stores are “full”, it acts to store the excess energy as fat (de novo lipogenesis).

When we haven’t eaten for a while or are sleeping, the hormone glucagon acts to break down the glycogen in our muscles and liver (glycogenolysis) in order to supply our brain and cells with glucose. Insulin acts to inhibit glucagon’s action, which signals the body to stop making new glucose from its glycogen stores. When our glycogen stores run out (such as when we are fasting), the body turns to non-carbohydrate sources such as fat to make the glucose it needs for essential functions (gluconeogenesis).

When we are insulin resistant, insulin continues to act on the liver to signal it to store energy. When glycogen stores are “full”, it stores the excess energy as fat. When fat stores are “full”, the body starts storing the excess fat that the liver keeps making, inside the liver itself.  There shouldn’t be fat in the liver, but when we are insulin resistant, such as in Type 2 Diabetes excess fat gets stored in the liver in a condition known as “fatty liver disease”.

In insulin resistance, the liver becomes more sensitive to insulin’s signal to make fat (and as a result keeps making more and more fat) yet at the same time, the liver becomes less sensitive to insulin’s inhibition of glucagon – resulting in more and more glucose being produced and released in the blood.

High levels of glucose remain in the blood despite adequate insulin, and it is this high level of blood glucose that is the hallmark symptom of Type 2 Diabetes. For the same quantity of insulin released, the body moves less and less glucose into the cell. 

What does the body do to compensate? It makes more insulin!

KEY POINT: Insulin resistance results in the increased production of insulin. Increasing blood sugar CAN a symptom, caused by the insulin resistance, but blood glucose can be normal and one can still be insulin resistant (see Featured Article on Insulin Resistance).

When we are insulin resistant and keep eating a carb-based diet, the body requires more and more insulin in order to move the same amount of glucose into the cell.

The main issue then becomes too much insulin (hyperinsulinemia).

Defining the Problem Defines the Treatment

In Type 2 Diabetes (which is in essence, very high insulin resistance), the symptom is high levels of glucose in the blood. That is not the cause. It is the symptom.

High levels of glucose in the blood resulting from uncontrolled Type 2 Diabetes, results in proteins in the body becoming “glycosylated”. Glucose, is a highly reactive molecule and easily accepts (or “shares”) electrons from other molecules – especially from the amino acid Lysine, which is found in virtually every protein in the body. When Lysine and glucose share an electron, it creates an irreversible chemical bond between the glucose molecule and the protein – and that protein is said to have become glycosylated. It is this glycosylation that lies behind the complications found in Diabetes.

To reduce the glucose in the blood and the glycosylation of the body’s proteins, current treatment for Type 2 Diabetes involves medications that move glucose from the blood into the cells. This doesn’t really remove the excess glucose from the body, it simply moves it to a different location in the body. While these medications can be very helpful in the short term (until people begin to address the underlying dietary causes), over time these medications become less and less effective at removing glucose from the blood. In a sense, we become “medication resistant”, so additional medications are added.  Once the various combinations of medications loose their effectiveness, people with Type 2 Diabetes are prescribed insulin as a treatment – because insulin moves excess glucose into the cells. But the cells are already overflowing with too much glucose!

Insulin is added as a treatment when the body is already producing too much insulin.  The problem is the cells aren’t responding to the signal from insulin. The body doesn’t need more insulin – it needs the cells that are sensitive to respond to insulin’s signal.

Diabetes as a “chronic, progressive disease”

Type 2 Diabetes is described as a “chronic, progressive disease” because with current medication treatment, people eventually get worse. When they no longer respond to the initial medications  prescribed that help move excess glucose from the blood into the cells, they are prescribed insulin which they take by injection – in order to force more glucose into already over-full cells.  While people’s blood glucose gets better (i.e. the symptom improves), they gain weight as a result of the insulin injections and develop complications such as heart disease, stroke, kidney disease, blindness etc..

In the end, they don’t get better, but worse, fulfilling the belief that T2D is a chronic, progressive disease.

Redefining the Problem, Redefines the Solution

Rather than looking at the symptom (high blood glucose) as something that needs to be “fixed” with medications and later with insulin (when the medications are no longer effective), when we define insulin resistance and Type 2 Diabetes as a problem of excess insulin, we approach addressing the problem differently.

By changing what we eat, we can lower the amount of glucose in the body, which in turn causes the body to produce less insulin.  With less insulin being produced, the cells begin to respond to normal amounts of insulin  – reversing insulin resistance and yes, reversing the symptoms of Type 2 Diabetes.

Eating a low carb high fat diet and extending the amount of time between meals (intermittent fasting) lowers the production of insulin, resulting in the cells become more sensitive to its signal. Rather than addressing the symptom (which is high blood glucose) we are addressing the problem of too much insulin.

Have questions? Would like to know how I could help you?

Why not send me a note using the “Contact Us” form on the tab above.

To our good health!

Joy

you can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

In Part 2, I will explain how insulin resistance is measured and how we can track insulin sensitivity returning, as we continue to eat a low carb diet and increase the time between meals.

Copyright ©2017 BetterByDesign Nutrition Ltd.  LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without regular monitoring by a Registered Dietitian and with the knowledge of your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing something you have read or heard in our content. 

 

 

 

Significance of Insulin Resistance

Insulin resistance is a condition where your body keeps producing more and more insulin in order to transport glucose out of the blood and store the excess by converting it to fat. When cells have become resistant to insulin, glucose builds up in the blood and results in “high blood sugar”. The problem is that high blood sugar is a symptom of the problem, it is not the problem itself.  Insulin resistance is the underlying cause and is highly significant to those with completely normal blood sugar levels.

Those with high fasting blood glucose may notice symptoms that are associated with Type 2 Diabetes; including excess urination and excess thirst. This is the body’s way of trying to dilute the high levels of glucose in the blood. A very sobering fact is that 75% of people with insulin resistance have normal fasting blood glucose levels and don’t know that they are insulin resistant.

They have NO symptoms whatsoever.

They don’t know that they are at increased risk for heart attack and stroke.

The Silent Risk of Insulin Resistance

Insulin resistance is a risk factor for atherosclerosis* – also called “hardening of the arteries”. Atherosclerosis is where plaque builds up inside the body’s arteries and if the plaque build-up occurs in the heart, brain or kidney, it can result in in coronary heart disease, angina (chest pain) or chronic kidney disease. These diseases are normally associated with Diabetes, but it is the underlying insulin resistance of Diabetes that creates the increased risk – not the high blood sugar itself.  Worthy of note, it is being insulin resistance that increases one’s risk – whether or not one also has high blood blood sugar.

The plaque that builds up in atherosclerosis may partially block or totally block blood flow to the heart or brain and if a piece of the plaque breaks off or if a blood clot (thrombus) appears on the plaque’s surface – this can block the artery  resulting in a heart attack or a stroke (in the brain).

Three quarters of people with normal fasting blood glucose are at increased risk of atherosclerosis and as a result, to heart attack and stroke due to insulin resistance and they don’t even know it, because their blood sugar is normal!

* a few recent references (there are many more): Pansuria M, Xi H, Li L, Yang X-F, Wang H. Insulin resistance, metabolic stress, and atherosclerosis. Frontiers in Bioscience (Scholar Edition). 2012;4:916-931. Santos, Itamar S. et al., Insulin resistance is associated with carotid intima-media thickness in non-diabetic subjects. A cross-sectional analysis of the ELSA-Brasil cohort baseline, Atherosclerosis 2017 Mar 10;260:34-40

Insulin Resistance with Normal Blood Glucose

Dr. Joseph R. Kraft, MD was Chairman of the Department of Clinical Pathology and Nuclear Medicine at St. Joseph Hospital in Chicago, Illinois for 35 years. He spent a quarter century devoted to the study of glucose metabolism and blood insulin levels.

Between 1972 and 1998, Dr. Kraft measured the Insulin Response to a carbohydrate / glucose load in almost 15,000 people aged 3 to 90 years old using a 5-hour oral glucose tolerance test with insulin assays. Data from 10,829 of these subjects indicated that 75% of subjects were insulin resistant — even though their fasting blood sugar level was normal.

That is, having a normal fasting blood glucose level, and normal HbA1C level does not preclude someone from being insulin resistant and at increased risk for heart attack and stroke.

The American Heart Association states on its web page that;

“exactly how atherosclerosis begins or what causes it isn’t known, but some theories have been proposed. Many scientists believe plaque begins to form because the inner lining of the artery, called the endothelium, becomes damaged. Three possible causes of damage to the arterial wall are (1) elevated levels of cholesterol and triglycerides in the blood (2) high blood pressure and (3) cigarette smoking”.

It is known that high triglycerides in the blood are largely a result of diets high in carbohydrates where excess carbohydrate that isn’t converted to glycogen and stored in muscle and liver is stored as triglyceride (three fatty acids attached to a glycerol molecule).

Insulin resistance in our cells, results in our bodies releasing more and more insulin in order to try to clear the same amount of glucose from our blood to store it in our liver as triglyceride (fat!). As covered in the blog post on the hormonal effect of insulin, it is the insulin which drives increased hunger and specifically increased craving for carbohydrates.  A viscous circle is created.  Diets that are 45-65% carbohydrate result in more and more insulin to handle the same carb load (that is the very nature of insulin resistance) and this increased insulin leads to even more insulin resistance, increased hunger and craving for….you guessed it: more carbs.

Since insulin’s main role is to store the excess glucose not needed immediately to fat – our bodies produce more and more triglyceride (fat!) the more carbs we eat and the more insulin resistant we are. That is, a high carb diet results in high triglycerides – which the American Heart Association recognizes as playing a role in the development of atherosclerosis. That is because triglycerides are converted to VLDLs to transport fat around the body and when their triglycerides ‘passengers’ are depleted, what is left is LDL, the “bad cholesterol” we have all heard about.  The ONLY source of LDL is VLDL, and high triglyceride is largely the result of a diet that is too high in carbohydrate.

Insulin also plays a significant role in the regulation of blood pressure through its effect on sodium transport. As insulin rises, excess sodium is retained by the kidneys, increasing blood pressure.  Insulin resistance compounds this problem, causing blood pressure to rise even more.  It has long been known that people with Diabetes develop high blood pressure – but it is the underlying insulin resistance that is driving that, not the symptom of high blood sugar.

What is alarming is that based on Kraft’s research with ~11,000 people over 20 years, potentially 75% of people are insulin resistant — even though their fasting blood sugar level is normal. This insulin resistance drives the increased triglycerides and high blood pressure that characterize what the American Heart Associations states is believed what underlies the development for atherosclerosis – and the corresponding risk of heart attack and stroke.

Could insulin resistance be a silent killer?

Kraft’s Patterns of Insulin Response

Kraft plotted the data from ~11,000 subjects and five distinct Insulin Response Patterns emerged.

Insulin Response Curves – image adapted from Dr. Ted Naiman

‘Pattern I: is a normal, healthy insulin response to a standard glucose load. Dr. Kraft called this ‘Euinsulin’.

image by Joy Y. Kiddie MSc RD
Pattern I: Normal Insulin Response Curve

Pattern II – is a hyperinsulinemic insulin response to a standard glucose. Note that Pattern II is considerably greater than the normal insulin response curve (Pattern I) and this greater insulin response is sustained for 5 hours after the ingestion of the glucose. 

image by Joy Y. Kiddie MSc RD
Pattern II hyperinsulinemia compared to normal glucose response (Pattern I)

Superimposing the hyperinsulinemic insulin response of Pattern II over the normal Pattern I insulin response curve, it is easy to see how much higher the Pattern II (yellow curve) is over the normal Pattern I (green) curve.  This is the early stages of insulin resistance.


Pattern III – is a hyperinsulinemic insulin response to a standard glucose load. Compared to the normal insulin response curve (Pattern I), it much greater during for 5 hours after taking in the glucose.

image from Joy Y. Kiddie MSc RD
Pattern III hyperinsulinemia compared to normal glucose response (Pattern I)

Superimposing Pattern III (hyperinsulinemia) insulin response curve over the normal (Pattern I) insulin response curve, its easy to see how the insulin response is delayed (skewed to the right). This results in blood glucose remaining high, as insulin is not responding as it should. Keep in mind, this is occurring in people with normal fasting blood glucose levels.

The Pattern III curve also goes so much higher than the normal Pattern I insulin response curve – which means that more insulin is released and this higher insulin release is sustained for the 5 hours after taking in the glucose.

This is “silent” pre-diabetes – delayed insulin response and much higher levels of insulin for a much longer time – but with normal fasting blood glucose!

Pattern IV – Pattern IV is what Dr. Kraft calls “Diabetes in Situ” – literally “Diabetes in Place”. Looking at the Pattern IV insulin response curve compared to Pattern I (the normal insulin response), it is apparent that it is much greater for the entire 5 hours after taking in a standard amount of glucose.

image created by Joy Y. Kiddie
DIABETES IN-SITU: Pattern IV insulin response points compared to the normal Pattern I insulin response curve (in green)
image created by Joy Y. Kiddie MSc RD
DIABETES IN-SITU: Pattern IV insulin response curve compared to the normal Pattern I insulin response curve (in green)

Surprisingly, 40% of people with a Pattern IV Insulin Resistance still had normal fasting blood glucose.

75% of people displaying Pattern II, II or IV insulin responses do not know that they are at greater risk for atherosclerosis and as a result to heart attack and stroke because they have no symptoms.  Their blood sugar levels are normal.

Finally, insulin resistance is the most common cause of Type 2 Diabetes.

Normal fasting blood glucose and normal HbA1C results do not reveal whether or not a person is insulin resistant – only a 2 hr glucose tolerance test can do that. Unfortunately, a 2 hour glucose tolerance test is usually only requisitioned when fasting blood glucose and HbA1C results come back abnormal.

Potentially, up to 75% of people are insulin resistance and have NO IDEA!

They are at increased risk for heart attack and stroke and have NO SYMPTOMS.

They don’t have increased thirst or increased urination like Type 2 Diabetics, but are at the same risk.

The Good News

The good news is, we can lower insulin resistance – and as a byproduct of that, shed excess weight in the process. This is accomplished through (1) a low carbohydrate diet with or without the use of (2) stretching the amount of time between meals (sometimes called “intermittent fasting”).

When designed properly, a low carbohydrate diet can provide all of the recommended intake of vitamin and minerals – while lowering insulin resistance.

That is where I come in.

I can assess your physiological needs for energy and nutrients and design an Individual Meal Plan that will enable you to lose weight, without being hungry all the time – and that will help lower your insulin resistance and the associated risk of cardiovascular disease related to insulin resistance.

Want to know more? Click on the “Contact Me” tab above and send me a note.

To our good health!

Joy

you can follow me at:

 https://twitter.com/lchfRD

  https://www.facebook.com/lchfRD/

Copyright ©2017 The Low Carb High Fat Dietitian (a division of BetterByDesign Nutrition Ltd).  LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without regular monitoring by a Registered Dietitian and with the knowledge of your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing something you have read in our content. 


follow me at:

 https://twitter.com/joykiddieRD

  https://www.facebook.com/lchfRD/