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: http://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: http://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.

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 webpage.

To our good health!

Joy


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


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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 glucoseInsulin 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

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.

 https://twitter.com/joykiddieRD

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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. 

 

 

 

Fasting Blood Glucose – the evening walk

As I’ve made it a habit to do each weekday, this morning I went out for my walk, using Nordic poles.  I had an appointment to keep, so I kept it to 3 km at a brisk pace, around that beautiful lake that I’ve previously posted a video update from.

Despite eating quite low carb and delaying the amount of time between meals each weekday, my fasting blood sugars remain high.  I’ve noticed that after I walk in the morning, they come down significantly, so I’ve decided to integrate a short walk around my neighbourhood after dinner, to see if my fasting blood glucose lowers.  It should, which leaves me to determine how long a walk is ideal. I don’t want to make it a “workout”, as that can interfere with sleep, but I also don’t want to make it so short that it doesn’t have any effect.  Today I started with a 15 minute walk at a comfortably brisk pace.  Tomorrow, I’ll try longer, to see if it changes the results in the morning, and if so by how much.

As I began my walk, I realized that I’ve lived in this neighbourhood for several years, yet never walk around it.  I guess it’s time I get to take in the beauty that is all around me.

Practicing what I preach!

Joy

UPDATE

It turns out, that a leisurely 20 minute walk after dinner results in my blood glucose dropping to ~5.2 – 5.4 mmol/L  (94-97 mg/dl) and staying that way through the night (measured at 1 AM and 4 AM and 6 AM in the interest of science, of course!).

This is now part of my routine!


 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.

A Dietitian’s Journey – what’s that on the floor?

This morning, as I was getting ready to go out for my walk, I noticed something on the floor.  As I started to bend down to pick it up, I realized it was my own toes! There they were – peeking out from under my shrinking abdomen! It shouldn’t be that the sight of one’s own toes while standing elicits such a surprised reaction, but it did.

As usual, I went walking this morning – something that has become a routine, since I fractured a rib 5 weeks ago (washing a bathtub, of all things!).  It was supposed to reduce the associated muscle pain (which it did) and after a few weeks, I realized I was really enjoying this “me” time, walking around a local lake. This week, I started Nordic walking (using Trek poles) and have really enjoyed the full-body exercise.  Even the drizzle wasn’t going to stop me today. After all, that’s what rain shells are for.  In fact, the one I grabbed this morning was the one I bought two years ago online, but that was too small, but today I put it on and zipped it right up. Finally, my body is changing! After 4 months of seeing very slow progress, the progress is becoming more and more evident.

Three weeks ago, at the encouragement of a local area physician whose practice focuses on low carb eating, I decided to take some body measurements, to track my progress.  I measured mid arm circumference  (between the point of my elbow and the pointy part of my shoulder blade), the my midpoint on my neck, my chest (where a brassiere would sit), my thigh (midway between my knee and my hip, at the widest part) and my abdomen at my umbilicus (or belly button) – which I have been tracking from the beginning.

[I don’t bother tracking my “waist” because this is smaller than the umbilicus, and what I want to assess is abdominal fat, which is better measured at the belly button.]

In the last three weeks, I’ve lost:

1/2 inch off my mid-arm

2 inches off my neck (yes I checked and rechecked this one!)

1 inch off my chest

1 inch off my umbilicus circumference

and gained 1/2 inch (of muscle) on my thighs.

Also during the last 3 weeks, I’ve lost 2 1/2 pounds and my fat percent has dropped 1.2%.

And today, I saw my toes!!

Yes, I have a long way to go, but I am not focusing on the destination but on the journey.  

I am enjoying eating real food and not feeling uncomfortably full afterwards (something absent since I gave up eat carb-based foods!).

I enjoy being able to delay the time between meals (intermittent fasting) without feeling hungry, tired, grumpy or deprived). Since I’m a Dietitian, I talk or write about food all day during the work week and most days I eat only supper.  Today I was hungry, so I ate a meal at 11am – but I still had a 16 hour ‘fast’ from supper last night until I ate today, where I hadn’t eaten anything. This time is so important, to enable my insulin levels to fall, and lower my insulin resistance that had been created by me previously eating 3 meals and 2-3 snacks per day, all centered around complex carbs – for years.

I like the feeling of being active; having gone from being totally sedentary (inactive) to being moderately active (45 minutes 5 days / week). I don’t exercise in order to lose weight, but because it is good for my heart and brain and it lowers my stress level (lowering cortisol).  This in turn is good for my blood pressure and for overall health. I enjoy doing it early in the morning and enjoying the feeling of well-being and satisfaction all day long.

For the first time in many years, I don’t eat because I am craving something, I eat because I am hungry!  In fact, I don’t crave anything!  I eat a small amount of dark chocolate each day (for health, of course) and even while intermittent fasting, I can walk through a bakery section of a store and not be the slightest bit interested in any of it.  My body is happily burning my own fat (which I have plenty of!) so I’m good.  I’m always drinking sparkling water (which I make at home) and usually finish 2 litres (a little less than 2 quarts) by the time I return from my morning Nordic walk.

I am sleeping so much better than I have in many years and have discontinued the prescription that I would keep on hand for the frequent nights I was unable to fall asleep. I still wake up sometimes because of my healing fractured rib (if I roll over) but other than that I wake up rested.  What a thought – waking up rested AND seeing my toes! I can get used to this.

Have questions?

Want to know how I can help you achieve your own health goals?  Why not send me a note using the “Contact Us” tab above.

To our good health!

Joy

 https://twitter.com/joykiddieRD

  https://www.facebook.com/lchfRD/


NNote: I am a "sample-set of 1" - meaning that my results may or may not be like any others who follow a similar lifestyle. If you are considering eating "low carb" and are taking medication to control your blood sugar or blood pressure, 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.

A Dietitian’s Journey – four month update (with lab test results)

It’s been 4 months since I began my own weight-loss journey, following a low carb high healthy fat diet and I’ve been to the lab and had my blood tests.  Here is an update on my progress to date.

Blood sugar

Fasting blood sugar

When I began this journey at the beginning of March, my fasting blood glucose was averaging 12 mmol/L – and this was when I was eating the ‘standard recommended diet’ for someone with Type 2 Diabetes. My diet was high in complex carbs, and low in saturated fat. Also, as has been traditionally recommended for someone with Type 2 Diabetes, I ate 3 meals per day and made sure to have 2 – 3 snacks per day (each with complex carbs and some protein).

Now, four months into eating low carb high fat, my fasting blood sugar is averaging 8.5 mmol/L. It is significantly better, but not what I had hoped which was to be at or below 6.0 mmol/L (below the Diabetic cutoff range) in this time.  There were factors that I was not considering.

Firstly, my blood sugar has been persistently high in the morning since I have been in nutritional ketosis – significantly higher than 2 hours after a meal.  At first, I couldn’t figure out why. I’d been tracking my blood glucose at various times of the day; fasting, before I eat, 2 hours after I eat, before bed etc., but regardless what I ate the night before, it was highest in the morning.  It was then that I began to suspect that the effect of the hormone cortisol might be a factor. 

Cortisol is our “fright and flight” hormone and under stressful conditions, such as being chased by someone or something, cortisol  provides the body with an immediate source of glucose by breaking down our glycogen stores in our muscle and liver (a process called glycogenolysis) and uses them to manufacture glucose in the liver (a process known as gluconeogenesis).

All hormones have a natural cycle of rising and falling throughout the day and this is known as a hormone’s circadian rhythm and over the course of the night, cortisol production begins to climb around midnight and reaches and is highest level between 6 am to 8 am.  When I began to track my blood sugar from 10 pm until 8 am, I noticed that it would start going up in the wee hours of the morning and keep rising until 6:30 or 7 am, am when I would take it. It was then that it became evident that my fasting blood sugar was rising with cortisol.

Chan S, Debono M. Replication of cortisol circadian rhythm: new advances in hydrocortisone replacement therapy. Therapeutic Advances in Endocrinology and Metabolism. 2010;1(3):129-138. doi:10.1177/2042018810380214.

When we sleep, our body breaks down the glycogen stored in our muscle and liver and converts it to glucose for our blood – an entirely normal process. Since I am following a low carb high fat diet and have been in nutritional ketosis for while, my body uses ketones as its primary fuel source and make all the glucose it needs for my blood from the protein and fat in my diet. When it runs out of that, it burns my stored fat for fuel – which is exactly what I want it to do! Since I’d been keeping my carbohydrate intake consistent but not very low, when cortisol levels would rise over night, my body would break down my glycogen first, then my own fat stores to make glucose for my blood, which I suspect is the origin of my high fasting blood glucose. That, combined with my liver still being insulin resistant, the glucose has no where to go.

This made sense to me and explained why my fasting blood glucose remained high, despite no carb creep (more carbs than planned for).

Since I’m keeping myself in nutritional ketosis, I’m not concerned about my fasting blood glucose remaining higher, although I may try distributing my carbs differently – with fewer at night. Since my goal is lower insulin resistance, I am going to continue to focus on that. High blood sugar is a symptom.  The problem is insulin resistance.

My blood glucose 2 hours after meals has been getting better. It is now averaging around 6.0 mmol/L (sometimes hovering around 5.5 mmol/L) which is much better than 7.2 – 8.6 mmol/L which is what it was at the beginning of March. My goal is to see it consistently below 5.0 mmol/L after meals by mid-November.

HbA1C – glycosolated Hemoglobin

Glycosolated hemoglobin (HbA1C) is the hemoglobin in our red blood cells that gets sugar molecules attached to it proportional to the amount of sugar in our blood. It is used to measure the three-month average plasma glucose concentration, based on the fact that the lifespan of a red blood cell is four months (120 days). The advantage of this test, is that one does not need to be fasting to have it.

HbA1C is most strongly correlated with fasting blood glucose (as opposed to pre-meal blood sugar or to 2 hour post-meal blood sugar) and since my fasting blood glucose has been consistently high, my HbA1C results naturally reflected this.  Lab tests indicate it is 7.5%, which is above the upper cutoff for Type 2 Diabetics of 7.0% – and higher than what I was aiming for, which was below 6.0%, the Diabetic range cutoff. However, since neither fasting blood glucose nor HbA1C  measure what I am trying to change (which is insulin sensitivity), I’ve decided that in November, I will pay to have my fasting insulin re-assessed.  After all, the goal is to lower insulin – which underlies the high blood sugar!

Lowering Stress

I knew that I needed to get my cortisol levels down, as cortisol drives appetite, which drives eating which in turn, causes insulin to be released. More insulin means my body will be focused on fat storage, not fat burning which is the opposite of what I want. Since my goal is lowering insulin resistance, lowering cortisol makes sense. Since I can’t change cortisol’s natural circadian rhythm, I had to focus on lowering the whole curve!  Lowering stress wasn’t going to happen sitting at my desk working. I had to get moving.  More on that, below.

Blood Pressure

As mentioned in my last update, a month ago I asked to be started on a very low dose of Ramipril (Altace), as my blood pressure had begun to creep up again. When I saw 160/90 mmHg two days in a row, I went to see my doctor.  He wasn’t there, but the locum agreed with my assessment that it was wise to protect my heart, brain and kidneys while I continued to make the dietary and lifestyle changes.  She asked me to delay getting my blood work for a few weeks, to assess my electrolytes (sodium and potassium) level which can be affected by the medication.

Even two years ago, my potassium was at the high end of normal – and this was when I was dutifully eating a diet high in complex carbs and low in saturated fat, as I ate a diet high in potassium-rich foods.

This time my potassium was at the upper normal limit, so I’m tracking my intake of it and keeping it approximately 1/3 to 1/2 of what it was previously.

Taking the blood pressure medication is a temporary measure that I decided on in order to offer some protection against heart attack, stroke and kidney damage until I lose more weight, and my blood pressure stays down on its own.

Thankfully, my overall kidney function is now better than it was 2 years ago, although I did need to make a few dietary changes to be sure that I avoid getting kidney stones (something that runs in my family).  When I started exercising regularly a month ago, I didn’t adequately increase my water intake – which I’ve since corrected.  I had also added a calcium supplement when I stopped drinking milk in March and which was binding with certain food components in the veggies and nuts I was eating.  This was probably what was resulting in calcium-oxalate being detectable in my urine. I’m no longer taking the calcium supplement and have added more hard cheese into my diet, instead.

Cholesterol

My LDL was at the high-end cutoff two years ago, but after 4 months on a low carb high healthy fat diet, it is approaching what is considered by the existing / popular standards of “optimal LDL” for someone who is high risk (family history of cardiovascular disease). My LDL is 2.60 mmol/L (1.14 mg/dl), my triglycerides (TG) were 0.64 mmol/L and my HDL was 1.97 mmol/L

Using more significant measures, my TG:HDL ratio is now 0.32 (with <0.87 considered ideal). According to several studies (that I will go into more detail in an upcoming article), a very low TG:HDL ratio is associated with lots of large, fluffy LDL – the kind associated the lowest risk of cardiovascular disease (CVD) such as heart attack and stroke. It is the higher density, small LDL particles that are associated with CVD.

Walking

A month ago, I began walking every morning during the weekdays.  I had just fractured a rib (slipping washing a bathtub!) and read that walking was good to reduce pain. Since reducing pain was high up on my “to do” list, I started with walking 1 km each morning during the week, before I began my office hours.  I gradually increased it to 2 km. The last week and a half it has been 3 km.

At the beginning of last week, I saw a fellow who was in very good shape using Nordic walking poles, so I asked him why he used them. He explained that as he digs the poles into the dirt on the path and pushes himself off of them, it gives him a good upper body as well as the lower body workout that comes from walking briskly. I decided to get myself some.

I researched what height they needed to be and decided whether I would get adjustable height ones or not, and purchased them on Friday and over the weekend, I read about how to use them properly. It seemed as thought it would be pretty intuitive for me, given that I have (and use) a Nordic Track ski machine when the weather is not conducive to going out to exercise.

Nordic Walking Poles

I was skeptical that using them could actually increase the calories I burned by 30%, for the same distance walked until I tried them this morning.

I am no longer skeptical!

I was very well aware of how much better a workout I had gotten after 2 km, but did another 1 km anyways.  I can’t wait to go again tomorrow.

Getting Even More Serious

Reducing Carbs

A month ago my weight was still ‘stuck’ at its 6 pound weight loss, so I decided to reduce my carbs slightly but consistently and to monitor my intake of nuts and dark chocolate, which could easily cause me to exceed my carb ceiling.

Bingo!

Intermittent Fasting

Monday – Friday I wasn’t hungry in the morning, because I would eat a very satisfying meal the night before (with adequate protein and lots of healthy fats and low carb veggies), so I was and am quite content to have only a coffee and cream for breakfast, and then go for my walk.

When I come home, most days I’m really not hungry, because my body had finally figured out how to burn my own fat stores for energy!

At first when I started exercising (nothing crazy…I was just walking briskly!) and delaying the time between meals, I needed to monitor my blood sugar even more often as it could get quite low in the late afternoon before dinner (+/- 4.0 mmol/L) – at which point I would eat something as I prepared dinner, to raise my blood sugar.

Here is a graph showing my blood glucose since I started walking and intermittent fasting;

Blood glucose since beginning walking and intermittent fasting

Weight Loss

In the last 3 weeks, my weight has dropped another 4 pounds, making it a total weight loss of 10 pounds, in all so far.  I expect as I continue to walk 4 days a week and intermittent fast most weekdays and limit my carbs, that the weight and inches will continue to come off.

I am not suffering in any way!

As a Dietitian, I talk about or write about food all day long and I’m intermittent fasting and feel just fine! I’m not hungry.  As I jokingly posted last week;

“My body has finally figured out how to make glucose from my fat on a low carb high fat diet. I may potentially have found the source of immortality.

Final Thoughts…

I still have at least another 30 pounds to go to get to the “goal weight” that I set at the beginning of this journey, and am now aiming to lose another 40-45 pounds instead in order to reach my ideal (healthiest) waist to height ratio. I clearly won’t accomplish this by mid-November, but if I reach close to my initial goal weight, I will be quite content.

They say a picture speaks a thousand words, so below are two photos. The one on the left, with the blue shirt is me at the beginning of this journey.  The one on the right, with the burgundy shirt is me now. I am starting to see a face I recognize.

Have questions?

Want to know how I can help you reach your own nutrition goals? Please send me a note using the “Contact Us” form above, letting me know how I can help.

To our good health!

Joy

 https://twitter.com/joykiddieRD

  https://www.facebook.com/lchfRD/

Note: I am a "sample-set of 1" - meaning that my results may or may not be like any others who follow a similar lifestyle. If you are considering eating "low carb" and are taking medication to control your blood sugar or blood pressure, 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.


 

Insulin and Leptin – very different effects in lean versus overweight people

The hormone insulin (involved in storing fat) and leptin (involved in burning fat) work very differently in lean people than in overweight people. This is why excess fat such as is found in “bullet proof coffee” or “fat bombs” results in overweight (or obese) people that follow a Low Carb High Fat diet gaining weight—whereas lean people will simply burn it off. This article explains the role of these hormones and how they impact lean people and overweight people very differently.

When we eat, the hormone insulin is released which signals our body to do two things; (1) it tells our cells to uptake energy (in the form of glucose) and (2) to store excess energy as fat. Insulin is the major driver of weight gain. If we are lean, when we eat more than usual and increase our body fat stores, the body responds by increasing secretion of a hormone called leptin.  Leptin acts as a negative feedback loop on the hypothalamus area of our brain, reducing our hunger, causing us to eat less and preventing us from gaining too much fat.

The problem occurs when we become insulin resistant.

Insulin Resistance

When we eat a diet that is high in carbs and we eat every few hours (3 meals plus snacks), insulin is released each time we eat (in order to cause our cells to take in energy and store the excess as fat). If we continue to eat this way, over time our body is inundated with insulin, so it sends signals to down-regulate the insulin receptors, making our cells less sensitive to insulin signals. This is called insulin resistance. When we are insulin resistant, our body releases more and more insulin to deal with the same amount of glucose in the blood.

Leptin Resistance

Consistently having high levels of insulin, will also keep stimulating the release of leptin, which normally results in us becoming less hungry and eating less. However, when we are insulin resistantwe keep producing more and more insulin, which results in us producing more and more leptin. Over time, this consistently high leptin level will result in the same type of down-regulation of hormonal receptors that occurred with insulin, resulting in leptin resistance.

Leptin resistance interferes with the negative feed back loop on our hypothalamus which normally reduces our hunger, causing us to eat less. When we are leptin resistance, even when we’ve eaten a great deal of food, we don’t feel satiated — even when our abdomens are straining from feeling full. As a result, we just keep eating, as if there is no “off” switch.

It is this leptin resistance that results in obesity. 

Obese people aren’t obese because they lack will-power, but because their body is responding to signals from very powerful hormones produced in response to the types of foods they eat.

Difference between a High Carb Diet and a High Fat Diet

When people consume diets high in carbs it stimulates insulin to be released. In response to all the insulin, energy that is not immediately needed for activity is stored as glycogen in the liver and muscle cells, and the remainder is shipped off to our adipose cells (fat cells), to be stored as fat. When eating a high carb diet, getting excess calories into fat cells is easy, getting the fat out of fat cells, not so much.

When people eat a diet high in fat and low in carbs, the fat is absorbed in the intestines as chylomicrons and is shuttled through the lymphatic system to the thoracic duct, going directly into the blood circulation. From there, the fat is either burned for energy or goes into our fat cells, to be stored. It is important to note that the fat does NOT go to the portal circulation of the liver and as a result, fat needs no help from insulin to be absorbed

That’s good, but if excess fat gets stored in fat cells, doesn’t eating fat make one fat?

Not for lean people, because lean people are leptin sensitive and obese people are leptin resistant. When overweight or obese people eat excess fat, it is a different matter.

Lean People versus Obese People

If a lean person eats a diet high in fat and low in carbs, the excess fat will be stored in fat cells, but insulin does not go up. So a lean person does not become insulin resistant, as described above.  As their fat mass goes up, leptin also goes up. Since the lean person is sensitive to leptin, the negative feedback loop acts on the brain causing them to stop eating, allowing their body weight to go back down. Even if a lean person deliberately eats more and more fat when they aren’t hungry, what happens is their body’s metabolism goes up, and they burn off the extra calories.

If an overweight or obese person eats a diet high in fat and low in carbs with moderate amounts of protein, insulin levels don’t go up — which is good of course, however from years of eating high carb low fat diets and from eating a carb rich foods every few hours, overweight and obese people are insulin resistant. This means that their blood glucose levels remain high for long periods after they’ve eaten and as importantly, it also means that they are also leptin resistant. In this case, if they eat too much fat – such as drinking “bullet-proof coffee” or having “fat bombs”, they will respond (as the lean person does) by making more leptin, but the problem is, they are not sensitive to leptin! Their brain doesn’t respond to the signals from leptin, so when an obese or overweight person eats excess fat, beyond that which is naturally found in a low carb high fat foods, their appetite doesn’t drop – nor does their metabolism go up to burn off the excess fat being stored in fat cells. They simply get fatter.

Weight Loss

For those that are overweight or obese and insulin resistant, it is important to keep in mind that with insulin resistance comes leptin resistance. Leptin resistance by definition means that the signals to stop eating don’t work.  The “off switch” is defective.  As well, the body doesn’t respond to signals from leptin to up-regulate metabolism, so when an overweight or obese person on a low carb diet eats too much fat, they gain weight.

Since increasing carbs is not an option and increasing protein results in glucose being synthesized from the excess (gluconeogenesis), the way to lower insulin resistance (and thus leptin resistance) is by extending the amount of time between meals.  This is known as intermittent fasting – a topic that will be covered in a future article.

Have questions?  

Want to know how I can help you get started on a low carb high healthy fat diet?  Please drop me a note using the “Contact Us” form, located on the tab above.

To our good health!

Joy

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 in our content. 


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References

Ebbeling CB, Swain JF, Feldman HA, et al. Effects of Dietary Composition During Weight Loss Maintenance: A Controlled Feeding Study. JAMA : The journal of the American Medical Association. 2012;307(24):2627-2634. doi:10.1001/jama.2012.6607.

Feinman RD, Fine EJ (2003) Thermodynamics and metabolic advantage of weight loss diets. Metabolic Syndrome and Related Disorders, 1:209-219.