Wednesday, March 30, 2011

Type 2 Diabetes - The Cause and The Cure


It's the disease that's becoming more and more prevalent among westernized cultures.  Diabetes, along with the obesity epidemic that's fueling it, is growing rampant and the numbers behind the illness are almost too large to wrap your mind around.  According to the American Diabetes Association (ADA) 25.8 million people have diabetes in the United States.  That's approximately 8.3% of the population.  But that's not the disturbing part.  The real kicker is another 79 million people in the U.S. are at risk for developing diabetes and are classified as having prediabetes.

The ADA goes on to report that the total cost of treating both diabetes and prediabetes in the U.S. in 2007 was a whopping $218 billion dollars!  That's more than the $171 billion dollars that the Department of Defense reportedly spent on BOTH the wars in Iraq and Afghanistan in 2010.  And it's almost double the $129.8 billion that the U.S. federal government budgeted for education in 2011.

But it's not the financial burden of diabetes that hurts the worst.  If you're one of the people who suffers from this chronic disease then you're probably all too familiar with the fact that diabetes can lead to further serious medical conditions including high blood pressure, heart disease, kidney failure, blindness, hearing loss, peripheral neuropathy, skin infections and skin ulcers, impotence, depression, peripheral arterial disease, strokes, limb amputations, and even death.  And with a list this long it goes without saying that we must do something to turn things around.  So what do we do?

First, we need to understand the disease better.  Second, we need to adopt the approaches that have been proven by science to be the most effective, safest, and least costly ways to beat this disease.  So what do you say... why don't we take an in depth look at both of these.


What's Happening Inside The Body Of A Diabetic?

There's been some fantastic research done to find out what's causing type 2 diabetes (T2D).  While we may not know every single answer, some things have been made unmistakably clear as to how this disease develops.  By understanding the following concepts you'll better be able to connect the dots when it comes to successfully preventing this disease or eliminating it all together if you currently have it.

1) Insulin Resistance

Insulin resistance is the topic that everyone is talking about from patients to diabetic educators to dietitians to the physicians who diagnose the disease.  It occurs when a person's fat, muscle, and liver cells don't respond appropriately to the actions of insulin.  Let's take a look at what insulin's job is in each one of these cells and how it's affected by insulin resistance.

Insulin and Fat Cells

Under normal conditions when we are in a fasting state our adipose tissue (body fat) undergoes lipolysis to provide the body with energy.  Lipolysis happens when triglycerides are broken down into free fatty acids (FFA) which are then released into the blood supply [1].  But when we are eating our pancreas produces insulin and this insulin suppresses lipolysis of our adipose tissue preventing the release of FFA into our circulation.  This makes sense because our body doesn't need to use its own fat stores for energy when we are eating because we can use the broken down glucose from the foods we're consuming.  However, in obesity insulin resistance prevents the suppression of lipolysis during the fed state and FFA (those tiny individual broken down particles of fat) are still being released into the circulation [2].  This leads to the redistribution of fat in our body to non-adipose tissues such as skeletal muscle cells and liver cells [3].


Insulin and Muscle Cells

After eating, the insulin in our bloodstream finds its way to an insulin receptor on the outer membrane of our muscle cells.  If everything is working properly, this insulin will start a cascade of signaling events inside these muscle cells to "open up" the doors of a glucose transporter called GLUT4 which also sits on our cell's outer membrane [4].  GLUT4 is responsible for transporting the glucose from our bloodstream into our muscle cells so that it can be used for energy [5].  Insulin resistance significantly decreases the ability of our muscle cells to perform this entire process.  This is a BIG, BIG deal because skeletal muscle is responsible for 70-90% of glucose disposal after eating a meal [4].  So if this chain of events isn't working properly guess what happens?  You got it - skyrocketing blood glucose levels!

Insulin and Liver Cells

In the liver, insulin plays a couple of roles.  First, after eating a meal it signals the liver to store extra glucose in the form of glycogen [6].  Second, when consuming a meal it tells your liver to stop breaking down the glycogen and other forms of glucose already stored in the liver since you don't need it because you're currently eating [6].  Insulin resistance disrupts these two processes which leads to extra glucose being dumped into the bloodstream.  This means higher blood glucose levels which is not what anyone is looking for.

2) Increased Intramyocellular Lipids (IMCL)

- Intramyocellular lipids (IMCL) are little particles of fat (i.e. free fatty acids - FFA) located inside muscle cells.  This is a very important topic when it comes to the pathogenesis of diabetes and one that many people including those in the medical field seem to be missing with the exception of Dr. Neal Barnard and a few others who have brought this research to light.

- All muscle cells have a small number of IMCL within them.  They're used for periods of time when your body doesn't have enough glucose available to meet your energy needs such as between meals.  However, a high amount of IMCL content in muscle cells has been linked to obese individuals displaying insulin resistance in multiple studies [7,8].  Type 2 diabetics, therefore, have an excess supply of IMCL in their muscle cells.  So why is this an issue?

- An over abundance of IMCL causes serious problems because they generate lipid metabolites known as diacylglycerol (DAG) and ceramide which interfere with insulin signaling [8,9].  DAG and ceramide impede the insulin signaling cascade that allows GLUT4 to transport glucose from the bloodstream into the muscle cell so it can be used for energy [4].  Consequently, there is an increased rate of insulin resistance seen in these patients which in turn keeps blood glucose levels high and type 2 diabetes raging out of control!  Needless to say, those extra tiny little particles of fat roaming around inside your muscles are a big reason why insulin resistance develops in the first place.

- One other detrimental effect worth mentioning is that an excess of IMCL lipid metabolites also activates pro-inflammatory substances leading to an inflammatory process within the body that has been linked as another cause of insulin resistance in cases of obesity and type 2 diabetes [10].

3) Reduction in PGC-1α

- What in the world is peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α)?  It's certainly a mouthful whatever it is!  PGC-1α actually plays an important role in the body and is responsible for regulating energy metabolism.  PGC-1α acts as a major activator of mitochondrial biogenesis [11].  Mitochondrial biogenesis just means the new formation of mitochondria within our cells.  This is important when it comes to our muscle cells because mitochondria act like little power plants located all throughout our cells and they're responsible for producing the energy needed by these cells to carry out their daily functions [12].  If mitochondria are considered the power plants of your cell then PGC-1α would be considered one of the chief engineers in charge of building these mitochondria.  That's a big responsibility indeed!  So why is building more mitochondria important?  Because mitochondria love glucose!

- Glucose is a key ingredient used by mitochondria to make energy and it's their primary source of fuel.  In obesity and T2D there is a reduced expression of PGC-1α [13,14].  And, unfortunately, if you have a smaller number of PGC-1α (chief engineers) then you have less mitochondria (power plants) in your cells.  This in turn leads to increased insulin resistance and a reduced ability to produce energy by your cells [4].  No wonder diabetes can wear people out and leave them exhausted.

How Can Type 2 Diabetes Be Prevented And Reversed?

Conventional medicine approaches type 2 diabetes with less than adequate advice on nutrition and exercise and a large emphasis on pills, pills, and more pills.  Throw in a little insulin when the pills stop working and you have yourself the typical type 2 diabetic patient just a handful of years after they've been diagnosed.

There's a reason for this.  That reason is because conventional medicine's approach with drugs is only trying to tackle diabetes on the back end by either increasing insulin production in the pancreas or by increasing insulin sensitivity of the various cells of the body.  The only problem with this approach is that T2D isn't just due to insulin resistance, as you've probably been told in the past, nor is it due to a lack of insulin production in the body.  Unlike antibiotics you take to cure infections, the medications you take for diabetes only slow down the progression of the disease.  They do not cure it.  While medications may be helpful in the short term to control your blood sugars they should only be relied on for just that purpose.  To get to the root cause of diabetes you have to remove the offending agents which are the foods that cause an imbalance in the cellular processes discussed above as well as a sedentary lifestyle.

It's kind of hard to win the war on diabetes when IMCL and mitochondrial biogenesis are left out of the conversation and on the sidelines like they're some kind of bench warmer who never gets in the ball game.  These bench warmers are significant playmakers in the "game" of T2D and the only way to prevent them from scoring for the other team is through proper nutrition and regular exercise.  The emphasis needs to primarily focus on nutrition as this is by far the biggest factor in defeating T2D.

Adopt A Low-Fat, Plant-Based Diet

If you were to pick one thing that could end your courtship with T2D it would be a nutrient dense, whole foods, low-fat, plant-based diet.  Eating wholesome, healthy foods will do your body wonders when it comes to tackling T2D.  You can completely get rid of T2D by consuming foods in the following categories from highest to lowest - vegetables > fruits > legumes > whole grains/nuts/seeds.  Keep in mind that it's just as important to stay away from processed foods, refined carbohydrates, and animal products (meat, dairy, and eggs).

The reason why you want to eliminate processed foods and animal products is because these items are much higher in fat and a high fat diets reek havoc on the body when it comes to T2D.  Even a diet high in fish consumption with the good fats (omega-3's) has been shown to increase your risk of developing T2D according to data covering a 16 year period from the Women's Health Study [20].

In contrast, plant-based foods are much lower in fat and will help prevent and even reverse T2D.  In addition, you will need to avoid oils (even olive and canola oil!) as all oils contain 100% of their calories from fat.  Avocados and nuts/seeds should be consumed only rarely in small quantities or avoided at least until you reverse your diabetes because these plant foods contain a large proportion of their calories from fat.  Here's the breakdown of how fat affects T2D:

- High fat diets have been linked to obesity-associated inflammation [15].  This leads to altered adipose tissue lipolysis and increases FFA in the bloodstream [4].  Remember that an over abundance of FFA (little fat particles) in the bloodstream leads to an increase in IMCL in the skeletal muscle further increasing insulin resistance as we talked about above.

- To the contrary, reducing saturated fats and high glycemic foods in one's diet leads to a reduced amount of IMCL concentration [16].  And reducing IMCL concentrations means reducing insulin resistance by reducing the amount of lipid metabolites available to interfere with the insulin signaling cascade as talked about previously.  So when you go on a low-fat, plant-based diet you actually give your muscle cells a fighting chance when it comes to utilizing the insulin and glucose in your blood which helps ward off T2D [16].

To put this in perspective let's take a look at the fat content of a typical plant-based meal from recipes off of PCRM's (Physicians Committee For Responsible Medicine) website compared to a meal made from recipes directly off the American Diabetes Association's website.  Keep in mind that low-fat plant based diets used to reverse T2D usually contain 10%-15% of their total calories from fat [17].  The typical American diet ranges from 20%-35% of total calories from fat which has never been shown to reverse T2D.

PCRM's Plant-Based Dinner
- Aztec Salad - 70 calories/serving, 9% calories from fat
- Black Bean Pueblo Pie - 177 calories/serving, 13% calories from fat
- Brown Rice and Barley - 111 calories/serving, 8% calories from fat
- Brownies - 48 calories, 6% calories from fat
- Beverage - Water
- Total calories - 406, Total calories from fat - 41 or roughly 10% of total calories from fat

American Diabetes Association's dinner
- Arugula and Watercrass Salad - 80 calories/serving, 70% calories from fat
- Mini Greek Chicken Kabobs - 60 calories/serving, 42% calories from fat
- Cheese and Rice Stuffed Peppers - 222 calories/serving, 17% calories from fat
- Cherry and Toasted Almond Pie - 232 calories, 37% calories from fat
- Beverage - Water
- Total calories - 594, Total calories from fat - 206 or roughly 35% of total calories from fat

So as you can see even a very prominent and highly respected organization like the ADA falls far short of giving the life saving advice that you need to successfully take on your diabetes.  And since most health care practitioners (doctors, diabetes educators, nurses, pharmacists, and even dietitians) rely on organizations like the ADA to lead the way in tackling T2D they too fall short of providing adequate guidance when it comes to treating T2D.  So how does the overall evidence stack up when it comes to a low-fat, plant-based diet in treating T2D?

A review of 14 randomized controlled clinical trials over a 10 year period showed that a low-fat, plant-based diet was more effective than other commonly used diets in treating T2D [19].  Individuals adopting a plant-based diet saw a marked increase in insulin sensitivity and glucose metabolism compared to the other dieters.  They also experienced greater improvements in their cholesterol levels, body weight, and hemoglobin A1C levels than the other dieters.

Choose Low-Glycemic Foods

One other important point in developing a successful diet plan for T2D is to make sure your foods are low on the glycemic index.  The glycemic index is a tool that shows how fast or slow a particular food increases your blood sugar after eating.  Foods high on the glycemic index tend to increase your blood sugar very rapidly and cause hyperglycemia while foods low on the glycemic index will tend to raise your blood sugar in a much more gradual and controlled manner minimizing the chances of hyperglycemia from happening.

Hyperglycemia has been shown to increase damage to your blood vessels, promote atherosclerosis, increase oxidative stress, and promote inflammatory processes in individuals with diabetes [18].  So it is vital that you stay away from high-glycemic foods such as white breads/pastas/rice, most cereals, pastries, and other high-glycemic foods.  To many people's surprise most all fruits are low on the glycemic index.

To learn more about this subject visit PCRM's page here.  You can also visit The Glycemic Index and look up any food you want and see how it stacks up in terms of the glycemic index.

Get Regular Amounts of Exercise

While nutrition is the main key to defeating T2D regular exercise also plays an important role.  Don't worry if you're one of those people who's frightened by the thought of having to spend hours in the gym.   That's not what I'm talking about.  As little as 30 minutes per day 5 days a week of moderate exercise (walking, swimming, biking, etc.) can have a big impact on taking back your health.  If you can't do 30 minutes at a shot then break it up into segments.  You'll get the same benefits from 10 minute segments as long as you do the same total amount of time each week.  The goal should be to get around 3 hours a week of moderate exercise.  Finding 3 hours out of a 168 hour week is so little when compared to the impact it can make on your overall health.  First though make sure you get your doctor's ok to start an exercise program especially if you have multiple health issues.  It's always better safe than sorry.

Why is exercise important?  There's a number of reasons so let's get to the details on exactly how it effects the way our body works on a cellular level.

- The combination of weight loss and exercise has been shown to decrease insulin resistance in patients.  This was shown in a study even though the amount of IMCL remained the same.  It was thought that the increased insulin sensitivity was due to a smaller droplet size seen of the IMCL particles which made them more usable in terms of breaking them down for energy production by the muscles cells [21].

- Skeletal muscle is made up of different types of muscle fibers known as type I fibers, type IIa fibers, or type IIb fibers.  Our genes, to an extent, determine which types of fibers our muscles will mostly consist of.  Type I fibers are great for endurance and produce energy more efficiently and therefore are great for running marathons or triathlons.  On the other hand type II fibers and even more specifically type IIb fibers are less efficient at producing energy but better for sprinting which requires only short bursts of energy.  Skeletal muscle cells of insulin resistant and obese individuals actually have about 30% less mitochondria and a higher content of type IIB fibers in them [4].  This is crucial because they are less able to dispose of the glucose available to them which exacerbates the effects of diabetes in these patients.  However, all is not lost because exercise has been shown to increase the number of mitochondria in cells, reduce insulin resistance, and improve hemoglobin A1c and fasting blood glucose results in patients with T2D [22].

- Another important role of exercise is it's ability to increase the amount of PGC-1α content in skeletal muscle [4].  If you remember PGC-1α is responsible for making more mitochondria inside our cells.  And the more mitochondria you have the more glucose that can be utilized in the process of making energy thereby improving your blood glucose levels.

- Moreover, an increase in PGC-1α expression due to regular exercise also helps convert some of those type IIb muscle fibers that aren't as efficient at producing energy into type I muscle fibers giving your body a tune-up so it becomes more proficient at using it's own glucose supply to produce energy [23].

The benefits of exercise have been made very clear by all the wonderful research out there.  Now that you understand exactly how it translates into improving your diabetes hopefully it will make it easier to stick with a regular exercise program.  After all, you deserve to feel your very best!

Summary And Final Thoughts

T2D can be a devastating disease not only financially for individuals and our nation as a whole but more importantly in terms of one's overall quality of life.  The additional health risks that come along with it can be crippling at best and deadly at worst.  But don't let this get you down because despite what you may have seen or heard, you are empowered to take this dreadful disease head on and turn it completely around.

Many experts have spoken up about insulin resistance and the important role it plays in the development and progression of T2D but this alone has only led to treatments and approaches that produce mediocre results at best.  Far too many patients and physicians are delaying the inevitable of further complications and disease progression with this approach alone.  That's because the other pieces of the puzzle have been missing.  These pieces include the crucial roles of IMCL and PGC-1α in the pathogenesis of T2D and hold the key to true success in eliminating this horrible disease once and for all.

Adopting a low-fat, plant-based diet along with a regular exercise program will put you back in the driver's seat when it comes to T2D.  And by doing so you'll be able to easily shed those extra pounds, start feeling better almost immediately, and in many cases eventually get off the medications that have only succeeded in giving you false hope of beating this disease.  You now have the knowledge and the understanding to do what thousands of doctors and millions of patients have never been able to do - SQUASH diabetes like it never existed!  Now go get 'em and prove to yourself and the rest of the world that you are not destined for a life of inevitable suffering.

I'll leave you with these additional resources to further help in your endeavors.

PCRM's Diabetes Website

Pursue A Healthy You

Dr. Fuhrman's Article on Reversing Diabetes Denied by the ADA For Publication Due to Eli Lilly Sponsorship

Dr. Montgomery Reverses Diabetes in Two of His Patients - Rosalee and Victor

Best of luck to all of you out there and please help spread the word that diabetes will one day be a thing of the past if we all just give a plant-based diet a try and stick to a healthier way of living.







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References:
1 Kolditz CI, Langin D. Adipose tissue lipolysis. Current Opinion in Clin Nutr & Metabolic Care. 2010 Jul;13(4):377-381.
2 Lelliott C, Vidal-Puig AJ. Lipotoxicity, an imbalance between lipogenesis de novo and fatty acid oxidation. Int J Obes Relat Metab Disord. 2004 Dec;28 Suppl 4:S22-8.
3 Unger RH, Orci L. Lipotoxic diseases of nonadipose tissues in obesity. Int J Obes Relat Metab Disord. 2000 Nov;24(4):S28-S32.
4 Eckardt K, Taube A, Eckel J. Obesity-associated insulin resistance in skeletal muscle: Role of lipid accumulation and physical inactivity. Rev Endocr Metab Disord. 2011 Feb;published online ahead of print. DOI:10.1007/s11154-011-9168-2.
5 Ezaki O. Regulatory Elements in the Insulin-Responsive Glucose Transporter (GLUT4) Gene. Biochem and Biophys Res Comm. 1997 Dec;241(1):1-6.
6 Foufelle F, Ferré P. New perspectives in the regulation of hepatic glycolytic and lipogenic genes by insulin and glucose: a role for the transcription factor sterol regulatory element binding protein-1c. Biochem J. 2002 September 1; 366(Pt 2): 377–391.
7 Aguer C, Mercier J, et al. Intramyocellular lipid accumulation is associated with permanent relocation ex vivo and in vitro of fatty acid translocase (FAT)/CD36 in obese patients. Diabetologia. 2010;53:1151-1163.
8 Moro C, Galgani JE, Luu L, et al. Influence of gender, obesity, and muscle lipase activity on intramyocellular lipids in sedentary individuals. J Clin Endocrinol Metab. 2009;94:3440-3447.
9 Adams JM, Pratipanawatr T, Berria R. et al. Ceramide content is increased in skeletal muscle from obese insulin-resistant humans. Diabetes. 2004;53:25-31.
10 Shoelson SE, Lee J, Yaun M. Inflammation and the IKK beta/I kappa B/NF-kappa B axis in obesity- and diet-induced insulin resistance. Int J Obes Relat Metab Disord. 2003 Dec;27 Suppl 3:S49-52.
11 Puigserver P, Wu Z, Park CW, et al. A cold-inducible coactivator of nuclear receptors linked to adaptive thermogenesis. Cell. 1998 Mar 20;92(6):829-39.
12 Voet, D, Voet JG, Pratt CW. Fundamentals of Biochemistry, 2nd Edition. 2006. John Wiley and Sons, Inc.. pp. 547.
13 Patti MF, Butte AJ, Crunkhorn S, et al. Coordinated reduction of genes of oxidative metabolism in humans with insulin resistance and diabetes: Potential role of PGC-1 and NRF1. Proc Natl Acad Sci USA. 2003;100:8466-8471.
14 Mootha VK, Lindgren CM, Eriksson KF, et al. PGC-1 alpha-responsive genes involved in oxidative phosphorylation are coordinately down regulated in human diabetes. Nat Genet. 2003;34:267-273.
15 Cani PD, Bibiloni R, Knauf C, et al. Changes in gut microbiota control metabolic endotoxemia-induced inflammation in high-fat diet-induced obesity and diabetes in mice. Diabetes. 2008;57:1470-1481.
16 Barnard ND, Katcher HI, Jenkins DJ, et al. Vegetarian and vegan diets in type 2 diabetes management. Nutr Rev. 2009 May;67(5):255-63.
17 Trapp CB, Barnard ND. Usefulness of vegetarian and vegan diets for treating type 2 diabetes. Curr Diab Rep. 2010 Apr;10(2):152-8.
18 Xu Y, He Z, King GL. Introduction of hyperglycemia and dyslipidemia in the pathogenesis of diabetic vascular complications. Curr Diab Rep. 2005 Apr;5(2):91-7.
19 Wolfram T, Ismail-Beigi F. Efficacy of high-fiber diets in the management of type 2 diabetes mellitus. Endocr Pract. 2011 Jan-Feb;17(1):132-42.
20 Djoussé L, Gaziano JM, Buring JE, Lee IM. Dietary omega-3 fatty acids and fish consumption and risk of type 2 diabetes. Am J Clin Nutr. 2011 Jan;93(1):143-50.
21 Jing HE, Goodpaster BH, Kelley DE. Effects of Weight Loss and Physical Activity on Muscle Lipid Content and Droplet Size. Obesity Research. 2004;12:761–769.
22 Toledo FG, Menshikova EV, Ritov VB, et al. Effects of Physical Activity and Weight Loss on Skeletal Muscle Mitochondria and Relationship With Glucose Control in Type 2 Diabetes. Diabetes. 2007 Aug;56(8):2142-2147.
23 Lin J, Wu H, Tarr PT, et al. Transcriptional co-activator PGC-1 alpha drives the formation of slow-twitch muscle fibres. Nature. 2002 Aug;418:797-801.

1 comment:

  1. Great blog! I like how you compared the cost of the wars to the cost of diabetes treatment. I'd like to find someone that eats a plant-based diet end up with type two diabetes. I bet they are a rare breed. Hopefully people take charge of their own health and begin to reverse this costly disease.

    ReplyDelete