Skinny Gene Project was a proud participant in the American Liver Foundation’s 16^th annual Liver Life Walk in San Diego.

Skinny Gene Project is a San Diego based non-profit focused on educating and empowering people who are prediabetic, or at risk for type 2 diabetes. At this event, Skinny Gene Project offered free information to participants, focusing on the connections between obesity and insulin resistance, which can be major factors for both diabetes and liver disease.

Here are a few of our pictures from the race…

The American Liver Foundation has been around since 1976 and focuses on research and education of liver diseases. The San Diego Liver Life Walk took place Saturday the 28th of June. Funds from this event go towards education and research of liver disease. The liver works together with your body to regulate the amount of sugar the body stores, and later how much of it gets released into the bloodstream. Therefore the liver plays a vital part in controlling blood sugars. Liver disease can cause many lasting complications, such as diabetes, kidney failure and loss of muscle mass.

Skinny Gene Project is an organization focused on the prevention of type 2 diabetes, giving advice for healthy lifestyle changes such as cooking and workout tips for free through their blog and social media accounts in order to reduce obesity, insulin resistance and high triglycerides. Skinny Gene Project also offers nutrition counseling services to people who are at-risk of type 2 diabetes.

Information about the American Liver Foundation: http://www.liverfoundation.org/about/

If you’ve watched any of the TED videos, you know that they are generally very thought provoking speeches that often challenge conventional thinking. Well, this video is no different. The question is simple…”Is obesity the problem” ; the answer is anything but.

Simply put, this video is not just thought provoking, it’s a great story. What begins as a snap judgement ends as a tearful plea for forgiveness. And in-between the two are a series of statements that really question how we view obesity and diabetes, and treat those with this very complicated metabolic disease.

Although we may not completely agree with all statements and conclusions made in this video, there are a few questions and points he raised that we absolutely stand behind. The 4 comments and statements below justify and reiterate why our work, as a non-profit diabetes prevention organization, in the community is still so desperately needed.

1. There isn’t a set dietary prescription for being insulin resistant and preventing diabetes.
   
2. Can people make the necessary changes in their diets in a way that’s safe and practical to implement? How can we move their behavior in that direction so that it becomes more the default rather than the exception?
3. Just because you know what to do doesn’t mean you’re always going to do it. Sometimes we have to put cues around people to make it easier.
4. We can’t keep blaming our overweight and diabetic patients. Most of them actually want to do the right thing, but they have to know what that is, and it’s got to work.

What points did he make that stood out the most to you?

TRANSCRIPT
I’ll never forget that day back in the spring of 2006. I was a surgical resident at The Johns Hopkins Hospital, taking emergency call. I got paged by the E.R. around 2 in the morning to come and see a woman with a diabetic ulcer on her foot. I can still remember sort of that smell of rotting flesh as I pulled the curtain back to see her. And everybody there agreed this woman was very sick and she needed to be in the hospital. That wasn’t being asked.The question that was being asked of me was a different one, which was, did she also need an amputation?

Now, looking back on that night, I’d love so desperately to believe that I treated that womanon that night with the same empathy and compassion I’d shown the 27-year-old newlywedwho came to the E.R. three nights earlier with lower back pain that turned out to be advanced pancreatic cancer. In her case, I knew there was nothing I could do that was actually going to save her life. The cancer was too advanced. But I was committed to making sure that I could do anything possible to make her stay more comfortable. I brought her a warm blanket and a cup of a coffee. I brought some for her parents. But more importantly, see, I passed no judgment on her, because obviously she had done nothing to bring this on herself. So why was it that, just a few nights later, as I stood in that same E.R. and determined that my diabetic patient did indeed need an amputation, why did I hold her in such bitter contempt?

You see, unlike the woman the night before, this woman had type 2 diabetes. She was fat.And we all know that’s from eating too much and not exercising enough, right? I mean, how hard can it be? As I looked down at her in the bed, I thought to myself, if you just tried caring even a little bit, you wouldn’t be in this situation at this moment with some doctor you’ve never met about to amputate your foot.

Why did I feel justified in judging her? I’d like to say I don’t know. But I actually do. You see, in the hubris of my youth, I thought I had her all figured out. She ate too much. She got unlucky. She got diabetes. Case closed.

Ironically, at that time in my life, I was also doing cancer research, immune-based therapies for melanoma, to be specific, and in that world I was actually taught to question everything,to challenge all assumptions and hold them to the highest possible scientific standards. Yet when it came to a disease like diabetes that kills Americans eight times more frequently than melanoma, I never once questioned the conventional wisdom. I actually just assmed the pathologic sequence of events was settled science.

Three years later, I found out how wrong I was. But this time, I was the patient. Despite exercising three or four hours every single day, and following the food pyramid to the letter,I’d gained a lot of weight and developed something called metabolic syndrome. Some of you may have heard of this. I had become insulin-resistant.

You can think of insulin as this master hormone that controls what our body does with the foods we eat, whether we burn it or store it. This is called fuel partitioning in the lingo. Now failure to produce enough insulin is incompatible with life. And insulin resistance, as its name suggests, is when your cells get increasingly resistant to the effect of insulin trying to do its job. Once you’re insulin-resistant, you’re on your way to getting diabetes, which is what happens when your pancreas can’t keep up with the resistance and make enough insulin. Now your blood sugar levels start to rise, and an entire cascade of pathologic eventssort of spirals out of control that can lead to heart disease, cancer, even Alzheimer’s disease, and amputations, just like that woman a few years earlier.

With that scare, I got busy changing my diet radically, adding and subtracting things most of you would find almost assuredly shocking. I did this and lost 40 pounds, weirdly while exercising less. I, as you can see, I guess I’m not overweight anymore. More importantly, I don’t have insulin resistance.

But most important, I was left with these three burning questions that wouldn’t go away:How did this happen to me if I was supposedly doing everything right? If the conventional wisdom about nutrition had failed me, was it possible it was failing someone else? And underlying these questions, I became almost maniacally obsessed in trying to understand the real relationship between obesity and insulin resistance.

Now, most researchers believe obesity is the cause of insulin resistance. Logically, then, if you want to treat insulin resistance, you get people to lose weight, right? You treat the obesity. But what if we have it backwards? What if obesity isn’t the cause of insulin resistance at all? In fact, what if it’s a symptom of a much deeper problem, the tip of a proverbial iceberg? I know it sounds crazy because we’re obviously in the midst of an obesity epidemic, but hear me out. What if obesity is a coping mechanism for a far more sinister problem going on underneath the cell? I’m not suggesting that obesity is benign, but what I am suggesting is it may be the lesser of two metabolic evils.

You can think of insulin resistance as the reduced capacity of ourselves to partition fuel, as I alluded to a moment ago, taking those calories that we take in and burning some appropriately and storing some appropriately. When we become insulin-resistant, the homeostasis in that balance deviates from this state. So now, when insulin says to a cell, I want you to burn more energy than the cell considers safe, the cell, in effect, says, “No thanks, I’d actually rather store this energy.” And because fat cells are actually missing most of the complex cellular machinery found in other cells, it’s probably the safest place to store it. So for many of us, about 75 million Americans, the appropriate response to insulin resistance may actually be to store it as fat, not the reverse, getting insulin resistance in response to getting fat.

This is a really subtle distinction, but the implication could be profound. Consider the following analogy: Think of the bruise you get on your shin when you inadvertently bang your leg into the coffee table. Sure, the bruise hurts like hell, and you almost certainly don’t like the discolored look, but we all know the bruise per se is not the problem. In fact, it’s the opposite. It’s a healthy response to the trauma, all of those immune cells rushing to the site of the injury to salvage cellular debris and prevent the spread of infection to elsewhere in the body. Now, imagine we thought bruises were the problem, and we evolved a giant medical establishment and a culture around treating bruises: masking creams, painkillers, you name it, all the while ignoring the fact that people are still banging their shins into coffee tables.How much better would we be if we treated the cause — telling people to pay attention when they walk through the living room — rather than the effect? Getting the cause and the effect right makes all the difference in the world. Getting it wrong, and the pharmaceutical industrycan still do very well for its shareholders but nothing improves for the people with bruised shins. Cause and effect.

So what I’m suggesting is maybe we have the cause and effect wrong on obesity and insulin resistance. Maybe we should be asking ourselves, is it possible that insulin resistance causes weight gain and the diseases associated with obesity, at least in most people?What if being obese is just a metabolic response to something much more threatening, an underlying epidemic, the one we ought to be worried about?

Let’s look at some suggestive facts. We know that 30 million obese Americans in the United States don’t have insulin resistance. And by the way, they don’t appear to be at anygreater risk of disease than lean people. Conversely, we know that six million lean people in the United States are insulin-resistant, and by the way, they appear to be at even greater risk for those metabolic disease I mentioned a moment ago than their obese counterparts.Now I don’t know why, but it might be because, in their case, their cells haven’t actually figured out the right thing to do with that excess energy. So if you can be obese and not have insulin resistance, and you can be lean and have it, this suggests that obesity may just be a proxy for what’s going on.

So what if we’re fighting the wrong war, fighting obesity rather than insulin resistance? Even worse, what if blaming the obese means we’re blaming the victims? What if some of our fundamental ideas about obesity are just wrong?

Personally, I can’t afford the luxury of arrogance anymore, let alone the luxury of certainty. I have my own ideas about what could be at the heart of this, but I’m wide open to others.Now, my hypothesis, because everybody always asks me, is this. If you ask yourself, what’s a cell trying to protect itself from when it becomes insulin resistant, the answer probably isn’t too much food. It’s more likely too much glucose: blood sugar. Now, we know that refined grains and starches elevate your blood sugar in the short run, and there’s even reason to believe that sugar may lead to insulin resistance directly. So if you put these physiological processes to work, I’d hypothesize that it might be our increased intake of refined grains, sugars and starches that’s driving this epidemic of obesity and diabetes, but through insulin resistance, you see, and not necessarily through just overeating and under-exercising.

When I lost my 40 pounds a few years ago, I did it simply by restricting those things, which admittedly suggests I have a bias based on my personal experience. But that doesn’t mean my bias is wrong, and most important, all of this can be tested scientifically. But step one is accepting the possibility that our current beliefs about obesity, diabetes and insulin resistance could be wrong and therefore must be tested. I’m betting my career on this.Today, I devote all of my time to working on this problem, and I’ll go wherever the science takes me. I’ve decided that what I can’t and won’t do anymore is pretend I have the answers when I don’t. I’ve been humbled enough by all I don’t know.

For the past year, I’ve been fortunate enough to work on this problem with the most amazing team of diabetes and obesity researchers in the country, and the best part is, just like Abraham Lincoln surrounded himself with a team of rivals, we’ve done the same thing. We’ve recruited a team of scientific rivals, the best and brightest who all have different hypothesesfor what’s at the heart of this epidemic. Some think it’s too many calories consumed. Others think it’s too much dietary fat. Others think it’s too many refined grains and starches. But this team of multi-disciplinary, highly skeptical and exceedingly talented researchers do agree on two things. First, this problem is just simply too important to continue ignoring because we think we know the answer. And two, if we’re willing to be wrong, if we’re willing to challenge the conventional wisdom with the best experiments science can offer, we can solve this problem.

I know it’s tempting to want an answer right now, some form of action or policy, some dietary prescription — eat this, not that — but if we want to get it right, we’re going to have to do much more rigorous science before we can write that prescription.

Briefly, to address this, our research program is focused around three meta-themes, or questions. First, how do the various foods we consume impact our metabolism, hormones and enzymes, and through what nuanced molecular mechanisms? Second, based on these insights, can people make the necessary changes in their diets in a way that’s safe and practical to implement? And finally, once we identify what safe and practical changes people can make to their diet, how can we move their behavior in that direction so that it becomes more the default rather than the exception? Just because you know what to do doesn’t mean you’re always going to do it. Sometimes we have to put cues around people to make it easier, and believe it or not, that can be studied scientifically.

I don’t know how this journey is going to end, but this much seems clear to me, at least.We can’t keep blaming our overweight and diabetic patients like I did. Most of them actually want to do the right thing, but they have to know what that is, and it’s got to work. I dream of a day when our patients can shed their excess pounds and cure themselves of insulin resistance, because as medical professionals, we’ve shed our excess mental baggage and cured ourselves of new idea resistance sufficiently to go back to our original ideals: open minds, the courage to throw out yesterday’s ideas when they don’t appear to be working,and the understanding that scientific truth isn’t final, but constantly evolving. Staying true to that path will be better for our patients and better for science. If obesity is nothing more than a proxy for metabolic illness, what good does it do us to punish those with the proxy?

Sometimes I think back to that night in the E.R. seven years ago. I wish I could speak with that woman again. I’d like to tell her how sorry I am. I’d say, as a doctor, I delivered the best clinical care I could, but as a human being, I let you down. You didn’t need my judgment and my contempt. You needed my empathy and compassion, and above all else, you needed a doctor who was willing to consider maybe you didn’t let the system down. Maybe the system, of which I was a part, was letting you down. If you’re watching this now, I hope you can forgive me.

Through my internship with the Skinny Gene Project, I had the opportunity to obtain a  better understanding of theses issues, and I‘d like to share my thoughts with you.

I’d like to begin with why I came to the U.S.

In South Korea I worked as a Process Engineer at a Pharmaceutical company. I wanted to change my profession and work for a global company, and to do so, I needed to improve my English. So I enrolled in the Intrax language school, because I could improve my English and gain experience interning at a U.S. company.

Life in San Diego

Living in San Diego has allowed me to create many memorable experiences that I wouldn’t have had in South Korea.  For example, San Diego keeps such a temperate climate throughout the year, it’s easy to take advantage of the ocean and go surfing, kayaking, and snorkeling.

Difference in Culture

From the moment I arrived here, the people were so friendly and hospitable to me all the time. This was very unexpected because, especially in my city, Seoul, it is not easy to imagine greeting strangers as if they have already known each other for a long time. What’s more, I couldn’t imagine a person I didn’t know approaching me and saying, “Hello”. I would think “why say hello to me? What is your intention?”

With its weather and friendly people, I see why everyone likes San Diego.

 Blended Culture

When I studied about American cultures, to prepare to come to San Diego, I heard that diabetes had become a growing issue in the U.S. Of course, diabetes is a big problem in South Korea, as well. The main reason Koreans think diabetes is a growing issue is because the Korean lifestyle is getting similar to the American’s lifestyle. Even we are consuming more foods like hamburgers, pizza and other fatty dishes, so we are starting to get some of the same health problems.

I’m curious, why do Americans have a bigger problem with obesity and diabetes than other countries?

In my opinion, I found two reasons to explain this. The first one, as mentioned above, is the “diet”.

I’ve had the unique experience of discussing the American diet with my friends from Intrax. It was surprising to hear their perspective, because the students are all from diverse countries like Brazil, Turkey, Korea, Japan, Germany and Taiwan etc., yet we all had the same opinion.

Unfortunately, nobody I spoke to thought “American foods” were healthy. My classmates said that most “American foods” had too much oil, and they believed many Americans eat these “greasy” foods all the time. Not sometimes. This way of eating appears to be a part of the American culture. This is the definite difference between the U.S and my country. It sounds like this is  also the difference between the states and my friend’s countries too.

In my country, we also enjoy something “oily”, but it can’t be always. It’s okay to eat in moderation.

The second reason why I believe Americans may have a bigger problem with obesity and diabetes is a lower level of physical activity. The U.S. has one of the best car markets in the world, which is why automotive companies from around the world love to sell to the U.S.  In other words, I think the driving culture is so well developed in the U.S. that it is easy to get anywhere by car. Whereas, in other countries, like South Korea, walking and public transportation are the main methods of transportation. Having a car seems nice, but on the contrary, I think it might be the core reason for the decreased level of exercise in the U.S.

Different Steps

In doing some research, I found an interesting fact.

According to the Pedometer Test, Americans take over 4,000 fewer steps (walking) a day than other countries.  This gap is equal to about 30 to 40 minutes of walking each day. It is recommended that people  in the U.S take at least 10,000 steps a day to maintain good health, which is approximately five miles of walking. The study showed that  on average Americans are only taking 5,117 steps a day.

This study surprised me, because it means American are getting half of the exercise they need to live a healthy lifestyle and prevent things like heart disease, obesity and diabetes.

Doing some quick math, I realized that these missing 4,000 + steps can really accumulate, causing a person to gain an extra 21 pounds a year.  These additional pounds can be the tipping point between a person being healthy and becoming overweight, getting  high blood pressure, or having  high cholesterol.  Or, it could even be the difference between a person with prediabetes developing full blown type 2 diabetes, or preventing it all together.

New Perspective

During the internship, I’ve been taught a lot of things that I’d not known and had misunderstood about obesity and diabetes. Especially, it was a good chance to learn the distinction between type 1 and type 2 diabetes, the important role diet and exercise can play in diabetes prevention, and most importantly that diabetes is no longer the disease for the older generation. People my age, late 20’s, need to start being more careful of their health and live a healthier lifestyle, if we want to prevent diabetes from continuing to attack our generation. It is becoming a global issue, but we don’t necessarily need a “big solution”. What I figured out from the research and lessons are that we can slow the growth of obesity and diabetes by taking small steps, 10,000 of them to be specific, to improve the health of all nations.

Before concluding my story, I want to say that San Diego is AWESOME. It not only helped me to achieve my prospective goals, but also provided a bunch of ways to broaden my horizons. I believe that all the experiences that I had in San Diego are invaluable and never forgettable.

To start us off, we asked Robert F. Dons, MD, PhD to share his thoughts  about the different terms used to describe diabetes or prediabetes.

I personally have had the pleasure of meeting Dr. Dons on a few occasions. Not only is he brilliant, he is also very kind.  It was apparent from our very first meeting that Dr. Dons cares deeply for his patients and goes above and beyond to ensure they are getting the best quality of care. I think what impressed me the most about Dr. Dons was his enthusiasm for patient education.  In addition to being one of the best Endocronologist I have met, here are some other fun facts about Dr. Dons.

• University of Illinois MD graduate 1973, PhD biochemistry graduate 1975
• Fellowship in Endocrinology, Diabetes and Metabolism at the National Institutes of Health 1982
• Private practice of clinical endocrinology for more than 10 years in San Antonio
• Published author of definitive textbook about tests used by endocrinologists for making endocrine diagnoses
• Endurance athlete –runner – working on 3^rd half marathon – projected finish time (62 years old)  in 2 hours 35 min

Please feel free to write questions about the article or Dr. Dons in the comment section below. 

Metabolic Syndrome or Pre-diabetes? NEITHER! What counts is “Early Diabetes”

Many folks have heard the term ‘borderline’ diabetes. Some have been told that is what they have. If you are one of them and have looked up what it means, you will probably come across the terms metabolic syndrome and ‘pre-diabetes’. You may see the term ‘early diabetes’ as well and that is what I wish to focus on in this article.

So what do all these terms mean? Do they all refer to the same thing or do they have significantly different meanings? Even more importantly, what is the underlying cause of these conditions, what does having one or more of these conditions mean in terms of future health and what can be done about them?

First, I would like to get rid of the term ‘borderline diabetes’. It can mean completely different things to patients and their doctors. In my opinion, the term is almost meaningless. One might use the phrase ‘sugar problem’ or a ‘touch of sugar’ and get the same level of information. In brief, serious problems with diabetes mellitus (DM) can be overlooked when this term is used or an over diagnosis of diabetes can be made when only a transient and insignificant change in blood sugar is detected.

Knowing something about sugar in the blood stream is important to understanding these terms. Sugar in the blood should always be called glucose. When measuring glucose the difference between glucose in the plasma versus that in whole blood must be understood. Whole blood is defined as plasma mixed with red cells; a plasma sample has had the red cells removed. Measurements done in laboratories on receipt of venous whole blood samples and those done from blood samples obtained from a finger may result in a report of either plasma or blood glucose level. In general, reports of plasma glucose are preferred since they are more accurate and have become the universal standard. These measurements are higher than those obtained from whole blood. The glucose levels used throughout the rest of this article will be those found in plasma.  

Many years ago, the term “Syndrome X’ was used to describe the mysterious coexistence of five medical problems which are now collectively called ‘metabolic syndrome’. They were hypertension, elevated fasting glucose, elevated triglycerides, low HDL and obesity. These problems are now precisely defined and are recognized as important markers of a serious, but common, condition known as insulin resistance. Much research has gone into understanding more about insulin resistance, but much more remains to be known.

It is important to know that having one or more of the features of metabolic syndrome does not mean that you are diabetic. On the other hand, most diabetics who are not dependent on insulin therapy have one or more of these problems. In the last few years, having one or more of these problems has led physicians to label a patient ‘pre-diabetic’. At first, some authorities thought that at least three of the five problems had to be present before this ‘diagnosis’ could be entertained. This idea was very arbitrary and has been abandoned. In my opinion, there is no practical set of features which defines a condition known as pre-diabetes. Thus, I discard this term much like the term ‘borderline’ diabetes.

So what are the features of metabolic syndrome? They are described in detail by the International Diabetes Foundation (IDF) and are presented in my book Endocrine and Metabolic Disorders Clinical Lab Testing Manual 4^th Edition 2009. In this book are described a multitude of other tests relevant to the diagnosis of diabetes mellitus (DM) and related conditions.

Precise definitions of the problems constituting the metabolic syndrome, as formalized in 2005, are as follows:

1. Hypertension with a systolic blood pressure or top number equal to or above 130 mm Hg or a diastolic or bottom number equal to or higher than 85 mm Hg
2. Elevated fasting plasma glucose on arising equal to or greater than 100 mg/dL
3. Elevated triglycerides, a lipid fraction in the blood, equal to or greater than 150 mg/dL, may be toxic to the beta cells of the pancreas by breaking up into free fatty acids.
4. Low HDL (high density lipoprotein), defined as less than 40 mg/dL for men and less than 50 mg/dL for women
5. Obesity, defined as an increase in abdominal girth (not waist size!) equal to or exceeding the gender and ethnic ‘cutoffs’ decided by the IDF, is perhaps the most important factor. These ‘cutoffs’ range from 37 inches for European men to 31 inches for Asian women. Other cutoffs popularly used in the U.S. are 40 inches for men and 35 inches for women.

At this point I would like to focus on the fasting and after meal glucose levels as markers of ‘early diabetes’. First of all it must be recognized that the term ‘early diabetes’ has not been precisely defined and that experts in the science of metabolism may argue for different definitions than I present here. Nonetheless, from my studies and experience, I believe that what follows is a practical and helpful guide to deciding if an individual actually has ‘early diabetes’.

When it comes to the fasting plasma glucose (FPG) level on arising from sleep, several factors must be taken into consideration. The first of these is the timing of the last intake of food or drink. While several hours (more than 2) is all it takes to bring the glucose into a ‘steady state’, a prolonged period of fasting (not eating or drinking anything, usually for more than 14 hours) can result in a falsely lower or non-diagnostic FPG. Another factor is the amount of fat stored in the liver. Higher amounts of fat are found in the livers of more obese persons and higher FPG will occur. Stress in general, sleep disturbances or sleep apnea syndromes also raise the FPG. If someone has absolutely no problem with diabetes or any of the other problems noted above, a normal FPG rarely is greater than 85 mg/dL. Early diabetes may be suspect at a FPG of greater than 94 mg/dL and is almost certainly present at 100 mg/dL or more while ‘overt’ DM is a level of 200 mg/dL or more.

So what about after meal glucose levels? It is important to differentiate these levels from ‘random’ glucose levels obtained anytime during the day. Scientifically, the after meal glucose is called a ‘post-prandial’ or post-cibum (pc) glucose and is measured in a blood sample obtained 2 hours from when the last meal was started. It is also important to recognize that this level is completely different from the glucose levels obtained after a glucose tolerance test or GTT. The GTT is a research test which involves the oral intake of an artificially high concentration of glucose (50 to 100 grams in water) over a short time followed by measurement of glucose levels at various times up to 5 hours. The GTT has only one use clinically and that is in pregnancy to help with the early diagnosis of gestational DM.

Post-prandial or pc glucose levels can go up in response to a variety of factors such as increased stress, high proportion of carbohydrates to protein and fat in the meal, a higher proportion of ‘simple’ to ‘complex’ carbohydrates in the meal, an inadequate number of calories eaten in the past few days followed by an excess carbohydrate intake, a faster rate of stomach emptying and a low-level of activity. However, when it comes to the diagnosis of early DM these factors are not critically important. Importantly, when an individual has a ‘normal’ FPG and abnormally high 2 hour pc glucose, the possibility of early DM is very likely.

If the 2 hour pc or random glucose level is 200 mg/dL or greater and is confirmed on repeat testing, the diagnosis of overt DM is established. Glucose values pc less than 200 mg/dL may or may not indicate DM. As a practical matter, in someone who is not known to be diabetic, a 2 hour pc glucose over 140 mg/dL prompts further study with repeat testing of the pc glucose and the use of another test called the hemoglobin A1c (HgbA_1c). It is not unusual for someone to have a single determination of pc glucose up to 180 mg/dL and not be diabetic especially if the factors noted above or diabetogenic (e.g., steroid) medications are involved.

In the diagnosis of early diabetes, the HgbA_1c is an invaluable, but occasionally misleading, test. The HgbA_1c allows an estimation of the average glucose level over the past 6 to 8 weeks. It is a fully integrated value reflecting both all the highs and all the lows in glucose. This test is capable of such a feat by using the capacity of the protein hemoglobin in red cells to combine with free glucose which binds to the hemoglobin in an irreversible manner. Thus, the higher the glucose level, the more binding and the higher the percentage of hemoglobin converted into HgbA_1c. While a truly non-diabetic level of HgbA_1c has not been established, the following cutoffs are of practical use. A HgbA_1c of less than 5.7% is not in the diabetic range unless the patient is anemic or has rapid turnover of red cells which falsely lowers the percentage of glucose bound to the hemoglobin molecule.  A HgbA_1c of 6.5% or greater is consistent with overt diabetes if other tests confirm it. HgbA_1c in between these levels are indeterminate, but highly suspect for the diagnosis of early diabetes especially if one or more features of the metabolic syndrome is present.

In summary, there are practical criteria for the diagnosis of early diabetes.  These criteria are a Hgb A_1c of between 5.8% and 6.5%, a confirmed FPG of more than 100 mg/dL, and a 2 hour pc glucose of more than 140 mg/dL. Once the diagnosis is made, treatment, particularly cost-effective lifestyle changes, can get started. This is important because bringing down the glucose can help preserve the insulin secreting capacity of the pancreas. Medications can help to accomplish this goal – an extension of the life of the pancreas. Lifestyle changes, particularly weight loss, help reduce triglycerides and its components known as free fatty acids which are toxic to insulin secreting cells in the pancreas.

(Disclaimer: Neither the  J.Moss Foundation nor the Skinny Gene Project  endorse any products or services offered by Women to Women. The information provided is strictly for education purposes only.)

Preventing type 2 diabetes and metabolic syndrome

by Marcelle Pick, OB/GYN NP

It’s sad to me that most of the women we see at our clinic either aren’t concerned about type 2 diabetes — or they already have it. I so wish that all women in the first group would learn from the women in the second. The key lesson is that your risk of developing type 2 diabetes is greater than you probably realize. The good news is you can prevent it, and the path to prevention will awaken you in so many ways.

I see patients who are not overweight and who think they’re leading fairly healthy lives end up with high blood sugar. In fact, some people who have prediabetes or metabolic syndrome are not obese, and may even be considered “thin.” Yet these women can go on to develop type 2 diabetes.

How does that happen? And how do you make sure it doesn’t happen to you? In my view, there are several factors behind the diabetes epidemic. Women don’t realize how much sugar — in all its forms — they are feeding their bodies. Of course, obesity and lack of exercise are enormous issues as well. But few people — and not many doctors — realize that diabetes is a metabolic disorder that has multiple causes.

Twenty years ago very few practitioners were aware of metabolic syndrome. In fact, it was a controversial idea. Today it’s a diagnosis that’s broadly accepted in conventional medicine. The new idea today is that there are many metabolic syndromes — a family of related disorders which lead to diabetes as well as to other chronic and degenerative diseases. That may sound scary, but it’s actually good news. It means that medicine is getting insight into how the body works, how to see problems much earlier, and how to prevent disease.

So let’s look into what you can learn now about your risks of developing type 2 diabetes — and how to make sure it doesn’t happen to you.

What is diabetes?

If I told you that people with untreated diabetes were literally starving, would you believe me? It may sound extreme, but it’s true. The term diabetes mellitus is actually derived from the Greek words meaning “to run through.” And this is exactly what’s happening. In diabetes, the nourishment we take in cannot get into our cells, and literally runs through the body instead of feeding it.

Think of feeding your hanging plants with too much nutrient-rich water. Instead of the roots drinking in the nutrients and water, the nourishment runs straight through the soil and trickles out onto the floor. No matter how much you feed the plant, the water runs through it. Eventually its leaves start to yellow, shrivel, or drop. Like your plant, the cells of a diabetic patient can’t absorb the nourishment they need.

Under normal circumstances, our bodies break down food we eat into potential energy. That energy enters the blood stream mostly in the form of glucose. Glucose is then escorted into our cells with the help of the hormone insulin, where it becomes the fundamental fuel for all cell activity. In diabetes, our cells can’t access glucose because insulin is either absent or unable to open the cell door to let it in.

The result is excess glucose or “sugar” floating around in the blood with no place to go. In a desperate effort to restore blood sugar levels to normal, our bodies end up eliminating the unused glucose, allowing it to “run through” our bodies, depriving us of the energy and nourishment we need.

Just as the leaves shriveling on your houseplant signal trouble, your body will try to alert you when it isn’t getting enough fuel. The following are warning signals that your body may already have type 2 diabetes:

• Increased hunger (especially in the form of carbohydrate cravings)
• Increased thirst
• Exhaustion
• Frequent urination
• Weight loss or gain
• Blurry vision
• Cuts or sores that won’t heal

Because your cells aren’t being fed, your brain sends out the message that you’re hungry, tired and thirsty. And though you may be eating and drinking more, your cells are literally starving. This faulty insulin signaling is the thread common to all forms of diabetes.

There are three main types of diabetes: type 1, type 2 and gestational diabetes. Type 1 is characterized by a defect in the islet cells of the pancreas that makes them unable to produce any insulin at all. Previously referred to as juvenile diabetes, type 1 is thought to be autoimmune in nature and is generally diagnosed in early childhood. Type 2, also commonly referred to as adult onset diabetes mellitus or noninsulin-dependent diabetes, develops when cells become resistant to insulin. And gestational diabetes occurs late in pregnancy when a mother’s hormones interfere with her ability to utilize insulin. All forms of diabetes, if left untreated, can lead to serious complications — including eye problems, compromised circulation, kidney damage, and nerve damage.

It may give you some comfort to know that type 2 diabetes doesn’t just hit overnight, but develops gradually over time. And though there are several risk factors that can increase your likelihood of developing it, the progression toward type 2 diabetes begins when you become resistant to your own insulin. In functional medicine, insulin resistance is an early indication of metabolic syndrome.

The connection between metabolic syndrome and type 2 diabetes

Twenty years ago, metabolic syndrome was almost an unknown idea among conventional practitioners. Today it is recognized as the precursor to full-blown diabetes. This is gratifying because it means conventional medicine accepts the idea that diabetes develops over time — it doesn’t just appear overnight.

The diagnosis of metabolic syndrome is made when three or more of five disorders are present in the patient: high triglycerides, low HDL cholesterol, high blood sugar, high blood pressure and an above-average waistline.

In functional medicine, insulin resistance and metabolic syndrome are the same thing. We view them this way because they begin with the same faulty cell signaling that, over time, causes metabolic disorders and damage, symptoms such as those used in the conventional diagnosis of metabolic syndrome, and eventually, degenerative diseases.

New research is showing that we can use specific nutrients to sort out the mixed-up cell signaling that occurs in metabolic syndrome and reverse the problem. This is fascinating to me because it promises that we can use food and supplements to prevent or reverse insulin resistance and other metabolic disorders instead of medication with its unwanted side effects! We will be hearing more about this in the next few years, but in the meantime following a Mediterranean diet can help provide similar effects.

Interestingly, making poor food choices is one of the big culprits leading to insulin resistance in the first place.

What causes prediabetes and the diabetes progression?

Type 2 diabetes manifests itself differently in each individual. And though symptoms and severity may vary, the starting point for most women is a diet with a high glycemic load (high in refined sugars and carbohydrates), combined with inactivity and a family history of type 2 diabetes. Next, the body reacts to high blood sugar by producing more insulin. With persistently high insulin levels, cells eventually build up a resistance to it and stop opening their doors. This stage, known as insulin resistance, is when glucose begins to pass through the body without being absorbed.

Soon enough, the pancreas gets the message and decreases insulin production. As insulin levels drop and diet remains high in glucose, blood sugar continues to creep up. Ultimately, insulin levels drop and blood sugar jumps dramatically. This is the point where the official diagnosis of diabetes is typically made. Since the harmful effects of insulin resistance cut across all the body’s systems, the severity at this point varies widely from individual to individual based on the health of their other systems. While some people with diabetes continue to make small amounts of insulin and can control their blood sugar through diet, others stop producing insulin altogether and have to rely on outside sources of insulin.

The progression is shown in the following diagram.

Numbers may differ from lab to lab, but type 2 diabetes is generally diagnosed when fasting blood glucose has reached 126 mg/dL or higher (compared to a normal range blood sugar level between 70 and 99 mg/dL). At Women to Women, we feel it’s much more beneficial to watch trends in blood glucose over time than to stick with one number.

In other words, if I see a woman’s blood glucose going up a little every year — even if those levels are still well under 99 mg/dL — I begin working with her right away to make healthy changes in her life. A gradual increase in blood sugar means that her cells are already insulin resistant, though the degree depends on her unique situation. And this is our chance to intervene early!

Fortunately, there are several stops on the pathway to type 2 diabetes and, as with any good road trip, there are various routes available and opportunities to turn around. The problem is that many conventional healthcare practitioners don’t step in early enough to change a patient’s course until it becomes difficult to reverse.

Waiting for sugar

It makes sense that if one out of every three of us is walking around with prediabetes, healthcare practitioners would be prepared to implement strategies to halt its progression to type 2. But this isn’t always the case. Standard blood tests look at blood sugar, among other things, but leave out one of the first indicators of prediabetes: insulin. Remember that insulin levels are among the first markers of change on the pathway to diabetes. At first they increase as insulin resistance sets in, then they start to decrease. So understanding how your insulin is working can help you to make important changes early on.

Sadly, many conventional practitioners lack the time to look closely at a patient’s lifestyle to determine if they could benefit from an insulin test. In fact, there is no set protocol for intervention until blood sugar begins to creep up, which means the patient has passed insulin resistance already. And though you can still reverse the problem, you’re much further along by then.

At Women to Women, we encourage our patients to take the driver’s seat when it comes to their health. Oftentimes, this means taking an honest look at your symptoms, nutrition and exercise habits, and it could also mean deciding for yourself that you could benefit from an insulin test. There is nothing wrong with requesting an insulin test from your healthcare provider yourself.

Staying on top of insulin early can help you avoid type 2 diabetes, insulin imbalance — and the problems associated with it, including imbalance of your sex hormones.

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Methodist Healthcare Ministries (MHM) is a non-profit organization dedicated to serving low income and uninsured families that would not qualify for federal or state programs that would provide such care. MHM invests well over $30 million annually to provide quality healthcare to the communities surrounding their 3 primary clinics. The Skinny Gene Diabetes Prevention Program will be implemented in two of these facilities, Wesley Health and Wellness and Dixon Clinic.

The Wesley Health and Wellness Center provides care for one of the most under-served populations in San Antonio. The area has nearly 100,000 individuals (90% Hispanic), of which more than half are 185% below the federal poverty guidelines. The Dixon Clinic provides medical and counseling services to a community on San Antonio’s east side, which has a large African-American population.

In 2009, Kevin Moriarty, President and CEO, expressed to the Skinny Gene Project his great concern for the growing obesity and diabetes epidemic that was affecting their communities. MHM has excellent programs in place to help their patients control their diabetes, but they realized a more aggressive approach would be needed  to fend off this disease. To better serve their communities, Kevin decided to take it take it one step further and implement a program that focuses on diabetes prevention.

As of April 2010, we are proud to announce that the Skinny Gene Diabetes Prevention Program is successfully being implemented at MHM. Over the next 12-months, our bilingual nutritionist (Nancy Juarez), under the supervision of our Senior Registered Dietitian (Emily Barr,MS,RD,CNSC), will be working one-on-one with a total of 15 patients to help them adopt healthy lifestyle changes and prevent the onset of type 2 diabetes.

Here are some of the new members of our Skinny Gene Family, San Antonio!

We’ve asked Nancy to share her experiences with us. Here’s what she had to say….

Methodist Healthcare Ministries (MHM) is a non-profit organization dedicated to serving low income and uninsured families. Their first and utmost interest is to provide the best quality healthcare they are able to offer to their patients. They provide medical, dental, and social services, along with a variety of activities, for the families they serve. They provide after-school care for children, whose parents work late, as well as computer and fitness classes for various ages ranging from children up to seniors. In the short period of time that I have worked in the MHM facility, it has opened my eyes to many possibilities and shown me the kind of help this organization can provide to its patients. Not only is there a sense of community, but there is also a real sense of family. A considerable number of families that benefit from MHM’s services are extremely grateful. If it wasn’t for MHM, these families wouldn’t have access to essential medical care, as well as the expensive medicines required to treat significant conditions and diseases. MHM has top-of-the-line equipment, which makes it possible for them to provide the best quality of care to each of their patients.

As a Skinny Gene nutritionist, I have been very lucky to have been given the opportunity to work with MHM. Since diabetes is a huge issue affecting millions of Americans in South Texas, this program will help these families by teaching them to make better food choices in order to achieve a longer and healthier life. We are currently making a difference in the lives of 15 individuals who are a part of our inaugural program at MHM. I am personally working with each of these wonderful people who are all grateful to Methodist for putting our Skinny Gene Diabetes Prevention Program in their lives. Each patient has an immediate family member or relative that has been diagnosed with diabetes, and after seeing the impact the condition has on their lives, want to prevent it from affecting them or their children.

Prior to this program, these patients (all at-risk of developing diabetes) had never been instructed by a personal nutritionist or dietitian on what they should or shouldn’t eat to lead a healthy life. Having the opportunity to have a nutritionist to guide them along the way to attain their goals is a dream to them.

All of these wonderful people are extremely motivated and excited to make very good use of what is being taught to them.

I have something in common with most of these patients—we come from Mexican descent.  As a bilingual nutritionist familiar with their culture and customs, I am able to communicate to them in a way that is meaningful and relevant to their lives. I am very pleased with the progress we have made in the short time we’ve had, but in time the difference will be noticeable and we will have paved the road for a healthier life.