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Is Keto For Everyone? Dr. Nally’s Three Principles of Health

Is a Ketogenic Lifestyle What Everyone Needs?

“Do I really need to be doing that ‘Keto Thing’?”

I get asked this question all the time.  And, my answer is that 85% of the people that walk through the doors of my clinic will not be fully successful in weight loss, reversal of diabetes, normalization of blood pressure and reversal of heart disease and/or vascular disease without it.

I am frequently asked, “Is Keto for everyone?”  Does everyone need to follow a ketogenic lifestyle?  The answer is “No.”  15% of the population will be able to maintain great health with calorie restriction and exercise.  However, the principles that provide a successful ketogenic lifestyle are easily understood and incorporated by anyone looking for improved health, energy and weight control.

Principle #1 – Insulin is the Master Hormone

Insulin is the master hormone when it comes to weight loss and the diseases of civilization. Whether you are insulin resistant or not, insulin is essential for life and proper function of the cells of the body, but too much insulin production in response to sugars, starches or complex carbohydrates causes disease.

How do you know if you are insulin resistant (producing too much insulin)?

Skin tags are pathognomonic (a characteristic indicative of the presence of disease) for insulin resistance. If you have skin tags, you may want to focus your diet on increased carbohydrate restriction.

You may not need to completely remove carbohydrate from your diet, however, recognizing that not all carbohydrates are created equal and avoiding those with higher carbohydrate content will help many improve weight and halt the progression of disease. I have many patients that with just partial carbohydrate restriction they are able to lose 20-30 lbs, improve their cholesterol profiles and improve their blood pressure.

There are sixteen different diseases that respond very effectively to carbohydrate restriction.  You can read about them and how the ketogenic lifestyle effectively reverses them in The Keto Cure.

Principle #2 – Saturated Fat & Cholesterol Aren’t the Demons We’ve Made Them Out to Be

Saturated Fat and cholesterol aren’t the demons we’ve made them out to be. Another way to put it is: “Don’t blame the butter for what the bread did.”

Since 1984, nutrition experts treat fat and cholesterol containing foods like the witches of Salem.  Experts castigate their use as if they were the “Avada Kedavra“ curse of the fantasy world.

As an example, eggs, specifically the egg yolk (the part of the egg containing all the cholesterol and saturated fat), have been demonized by just about every health magazine I’ve ever read. (To this day, the chef at every breakfast bar I’ve ever visited asks if I want an ‘egg white only’ omelet.) Interestingly, there is actually no scientific data association between whole egg consumption and heart disease. The science simply does not exist. Seriously, check for yourself.

I personally eat 6-8 eggs a day and my cholesterol is perfect. Back 1000 years ago, only the aristocrats at the chickens.  All laborers and serfs ate the eggs . . . who would be dumb enough to eat your food source? (Don’t answer that.)

For example, the MR-FIT study, the largest cholesterol study ever completed, is incessantly quoted as the study that demonstrates reduction in cholesterol leads to reduction in cardiovascular disease, but this trial was actually a failure and did not demonstrate improved risk by lowering cholesterol. In fact, the Director of the study, Dr. William Castelli stated, “. . . the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower people’s serum cholesterol…”

Researchers found that people who ate the most cholesterol, including the most saturated fat, weighed the least. They were also the most physically active. In fact, the British Medical Journal published a 2015 study demonstrating that saturated fat is NOT linked to vascular disease, diabetes or increased mortality (de Souza RJ et al., BMJ 2015,351:h3978).

In my clinic, the basis of appetite suppression is eating adequate protein that includes saturated fat and cholesterol. This is the most powerful tool in my clinical approach to the treatment of weight loss.  I can use foods like red meat, bacon, butter and coconut oil without concern or worry of heart disease as long as you are keeping your carbohydrate intake less than 20 grams per day.

Baseline insulin levels allow for peace of mind about heart disease risk. Heart disease risk goes down when insulin levels are maintained at normal baseline levels. Increasing saturated fat, while at the same time lowering carbohydrate intake has been demonstrated to shift the cholesterol to a more heart protective form (Griffin BA et al., Clin Sci [Lond], 1999 Sep).

Principle #3 – Nutritional Ketosis Has Anti-Inflammatory & Age Slowing Effects On the Body

Ketones in the blood at a nutritional level (0.5-4 mmol/L) have tremendous anti-inflammatory and age slowing effects on the body.  Even having them present intermittently has dramatic improvement on overall inflammatory changes and disease in the body.

Ketones are the usable fuel of the body when the liver breaks down fat for energy. They suppress the NLRP3 inflammasome in every cell in the body. This is important because it allows for more rapid recovery from exercise. It also dramatically decreases pain and fatigue that comes from diseases like arthritis, rheumatoid arthritis, multiple sclerosis and auto-immune disease (Y.H. Youm, et al., Nature Medicine, vol. 21, no. 3, pp. 263–269, 2015.)

If full blown ketosis isn’t for you, partially restrict starch and carbohydrates for a mild to moderate benefit.  Even small amounts of ketones in the blood are helpful.  This provides increased recovery time, and improved inflammation control.

So, even if you don’t follow a strict ketogenic lifestyle, the principles above are powerful.  These three principles make this dietary approach universally effective for weight loss.  They are also very powerful for disease management.  Even partial application of carbohydrate restriction can benefit just about everyone.

You can learn much much more about the Ketogenic Lifestyle as a member of DocMuscles.com.  Click the link and sign up now.

And, don’t forget to get your signed copy of my book, The Keto Cure.

What Blood Tests are Important In a Ketogenic Lifestyle?

So, you’ve started a ketogenic lifestyle and you’re a few months in . . . but, is it really working? How do you know? You should be seeing your waist shrink. But, is all that butter really good for my cholesterol? What about my blood tests?

I commonly get these questions over the last 12-13 years of using a low-carbohydrate or ketogenic lifestyle approach in the treatment of obesity, diabetes, cholesterol and high blood pressure. We can determine the effectiveness of the diet on your metabolism with some simple blood testing.

What Lab Tests Do You Need?

Watch the video below to find out what tests are right for you:

Why don’t you check all the other inflammatory markers like HS-CRP, Lp(a), etc?  Because, I know that these test will be elevated if insulin is > 5 mmol/L and if sdLDL particle is > 500 nmol/L.

Check out our membership site and the benefits that come with it.

Salt #DocMuscles #KetonianKing DocMuscles.com

What If Salt Actually Improves Blood Pressure & Blood Sugar?

What if increasing your salt intake actually improved your diabetic blood sugar?

What if increasing salt intake actually lowered your blood pressure?  Could it be that easy?

Just about every patient that I see has significant worry about salt intake.  Some greater than others. In fact, some people are so salt phobic that when I encouraged its use, they called me a “quack” and left my practice.  But does salt restriction really work, or is it doing more damage than we think?

That was the question that was asked by Dr. Ames in the American Journal of Hypertension 17 years ago.  However, his answer never got a mention.  In fact, I’ve been in practice for almost 18 years, and incidentally stumbled upon this article when it was mentioned by a colleague of mine.   Granted, it is a small sample of people, only 21 in the study.  However, the results are profound.

21 patients with hypertension were randomized to periods of no salt (placebo) and periods of 2 grams (2000 mg) of sodium chloride four times a day (a total of 8 grams of salt per day).  Glucose tolerance tests were completed with insulin levels at the end of each intervention period.

Insulin Resistance and Hypertension Improve by Adding Salt

What was noteworthy was that those with insulin resistance and diabetes had improvement in their glucose levels while on sodium supplementation.  Those with hypertension had improvement in their blood pressure while on the sodium supplementation.   Lastly, those with insulin resistance had a lowering of their insulin levels during the period of increased sodium intake.  These findings fly in the face of the dogma that’s been drilled into our heads that “salt is bad!”

“But, you can’t base your findings on a small group of 21 people,” the experts say.

Yes, it is a small study group. However, these findings are what I, also, have seen clinically in my practice for over 13 years.

We know that the average human needs 3 grams of sodium per day and 3 grams of potassium per day.  If you’re eating the standard American diet (SAD diet) including processed foods, you’re getting 2-3 grams per day of sodium.  In fact, the CDC claims the worst meals for you are:

  • Bread
  • Processed chicken dinners
  • Pizza
  • Pasta

However, if your following a low-carbohydrate or ketogenic lifestyle, you won’t be eating the meals above and you’re probably not getting near enough salt.  This is the cause of the keto-flu I wrote about a few weeks ago.  And, according to the study above, it is a potential driver of our persisting insulin resistance, diabetes and hypertension.

How Much Salt Should I Use?

In my office, I encourage use of 3-4 grams of sodium and 3-4 grams of potassium daily when using a ketogenic lifestyle.  That’s approximately 1 1/2 – 2 teaspoons of salt per day.  I like Redmond’s RealSalt or if you can’t find it, Himalayan Pink Salt, because the pink sea salts contain sodium, potassium, magnesium and zinc.

Could it be that salt restrictions are making our insulin resistance and blood pressure worse?  That’s what the clinical evidences are pointing toward. However, more research is still needed.

Want to know more about a ketogenic life-style?  Click the link on KetoLife above to get some basics.  If you’re already following a ketogenic lifestyle, then let me help you navigate the bumps and turns by going to the Supplement section above and checking out the products I recommend to jump-start ketosis DocMuscles style!

Until then, I’ll have another piece of bacon, please . . . and, oh, pass the salt!

Type II Diabetes Mellitus through the Lens of Insulin Resistance

Watch as we discuss Type II Diabetes from the perspective of insulin resistance and how using a ketogenic diet/lifestyle as well as exogenous ketones, KetoEssentials Multivitamin and supplements like berberine play a role in improving your health.

Grab your bacon, butter and pecans, . . . pull up a chair, and enjoy!!

Ketogenic Lifestyle Rule #3: Be BOLD or Be Italic, but never be Regular: Why Size Matters with Cholesterol


On this evenings PeriScope video we talked about cholesterol.  And, and you can see an updated, in depth discussion about cholesterol on my YouTube channel here.  Please go check it out and if you find it helpful, please follow me here and on YouTube.   The is the burning question on everyone’s mind who starts a Low-Carb, High Fat or Ketogenic Diet: “What will happen to my cholesterol if I lower my carbohydrates and eat more fat?”

The answer . . . it will improve!

How do I know this?  I’m an obesity specialist.  I specialize in FAT or lipids (to put it kinder scientific terms).  To specialize in fat, one must know where it came from, what it’s made of and where it is going. And,  this has been the case with every single patient I have used this dietary change with for the last ten years, myself included.

Lets start with the contents of the standard cholesterol or “Lipid Panel”:

  • Total Cholesterol
  • HDL-C (the calculated number for “good” cholesterol)
  • LDL-C (the calculated number for “bad” cholesterol).
  • Triglycerides

The first problem with this panel is that it makes you believe that there are four different forms of cholesterol.  NOT TRUE!  Actually cholesterol is cholesterol, but it comes in different sizes based on what it’s function is at that moment in time.   Think of cholesterol as a bus.  There are bigger busses and smaller busses.   Second, triglyceride is actually the passenger inside the HDL and the LDL busses.  And third, Total Cholesterol is the sum of the HDL, LDL, as well as ILDL & VLDL which aren’t reported in the “Lipid Panel” above.

The fourth thing that this panel doesn’t tell you is that HDL & LDL are actually made up of sub-types or sub-particles and are further differentiated by weight and size.

Cholesterol Size

For our conversation, we need to know that the number of LDL particles (LDL-P) can actually be measured in four different ways and these measurements have identifed that there are three sub-types: “Big fluffy” large dense LDL, medium dense LDL, and small-dense LDL.  Research has identified that increased numbers of small-dense LDL correlates closely with risk for inflammation, heart disease and vascular disease (1).

Microsoft PowerPoint - ADA Otvos LDL size talk_modified.ppt [Com

If you’ve been a follower of my blog for a while, you’ve seen this picture before. This picture illustrates why an LDL-C (the bad cholesterol measurement) can be misleading. Both sides of the scale reflect an LDL-C of 130 mg./dl. However, the LEFT side is made up of only a few large fluffy LDL particles (this is the person with reduced risk for heart disease) called Pattern A  or a LDL healthy cholesterol level.  Even though the LDL-C is elevate above the recommended level of 100 mg/dl, the patient on the left has much less risk for vascular disease (this is why you CAN’T trust LDL-C as a risk factor).

The RIGHT side of the scale shows that the same 130 mg/dl of LDL-C is made up of man more small dense LDL particles (called “sd LDL-P”) with a Pattern B type that is as increased risk for heart or vascular disease.  This is where the standard Lipid Panel above, fails to identify heart disease and it’s progression.

Research tells us that the small dense LDL particle levels increase as the triglycerides increase.  And we know that Triglyceride levels increase in the presence of higher levels of insulin leading to a cascade of inflammatory changes.  Insulin is directly increased by the ingestion of simple and complex carbohydrates.  Insulin also increases with the ingestion of too much protein.  So, that chicken salad or the oatmeal you ate, thinking it was good for you, actually just raised your cholesterol.   If you are insulin resistant, your cholesterol just increased by 2-10 times the normal level (see my article here on how insulin resistance causes this.)

Adapt Your Life

“Ok, but Dr. Nally, there are four different companies out in the market measuring these fractional forms of cholesterol. Which one should I choose?”

There are actually five different ways you can check your risk.

  1. Apolipoprotein levels.  This can be done through most labs; however, this test doesn’t give you additional information on insulin resistance that the other tests can.
  2. Berkley Heart Lab’s Gradient Gel Electrophoresis – This test gives a differentiation based on particle estimation between Pattern A and Pattern B
  3. Vertical Auto Profile (VAP-II) test by Arthrotec – This test determines predominant LDL size but does not give a quantifiable lipoprotein particle number which I find very useful in monitoring progression of insulin resistance and inflammation.
  4. NMR Spectroscopy from LipoScience – This test measures actual lipoprotein particle number as well as insulin resistance scores and will add the Lp(a) if requested.  I find the NMR to be the most user friendly test and useful clinically in monitoring cholesterol, vascular risk, insulin resistance progression and control of the inflammation caused by diabetes.  This test has the least variation based on collection methods if frozen storage is used.
  5. Ion-Mobility from Quest – This test also measures lipoprotein particle number but does not include insulin resistance risk or scoring.  Because the test is done through a gas-phase electric differential, the reference ranges for normal are slightly different from the NMR.

In regards to screening for cardiovascular risk, the use of all five approaches are more effective than the standard lipid panel.  However, I have found that clinically the NMR Lipo-profile or the Cardio I-Q Ion-Mobility tests are the most useful in additionally monitoring insulin resistance, inflammation, and disease progression.

It is was the use of these tests that demonstrated to me the profound effect of carbohydrate restriction and ketogenic lifestyles on vascular and metabolic risk.  We talk more about these tests on my YouTube video .

Hope this helps.

KetoOS Image

References:

  1. Williams PT, et al. Comparison of four methods of analysis of lipoprotein particle subfractions for their association with angiographic progression of coronary artery disease. Atherosclerosis. 2014 April; 233(2): 713-720.

Patience: Why Weight Loss is a Slow Process?

tortoise_&_hare_1

Watch this weekend’s Periscope conversation about why weight loss is slow and why anything that is worthwhile takes time.

You can watch the Periscope Video below:

The Ketogenic Diet & Multiple Sclerosis

Multiple Sclerosis (MS) is a neurological disease caused by demyelination or breakdown of the myelin coating around the nerve cells (1).   This is referred to as a neurodegeneration where the physical structure of the nerve is compromised, much like the coating around an electrical wire being chipped or stripped away. Common symptoms of MS are sensory symptoms in the extremities or face, unilateral visual loss, acute or subacute motor weakness of the muslces, diplopia (double vision), gait disturbance and balance problems, Lhermitte sign (electric shock-like sensations that run down the back and/or limbs upon flexion of the neck), vertigo, bladder problems, loss of control of a limb,  and pain.

 

Effects of Ketosis on Multiple Sclerosis

Initially, and for many years, the degeneration seen in multiple sclerosis (MS) was thought to occur because of an acute inflammatory attack on the cells by dis-regulated immune cells crossing the blood brain barrier.  However, treatments focused on modulating the inflammatory attack seem to have no effect on the degeneration and demyelination.  Thus, the actual definitive cause of this demyelination and neuro-degeneration has eluded us since 1868, when Jean-Martin Charcot first described it.

Recent studies point to evidence that this demyelation may be due to degeneration or breakdown of the nerve cell’s ability to use glucose as a primary fuel (2, 3).  It is now theorized that MS may be due to a combination of degeneration and localized inflammation related to poor glucose uptake causing the demyelination which is seen in a number of MS cases (4, 5, 6).

Demyelination of Nerve
A. Normal nerve cell with intact myelin sheath around the axon. B. Demyelinated axion nerve losing its ionic charge due to escape of potassium. C. Radio-labled tracer allowing visualization of demyelination on PET Scan

With this dual concept in mind, ketogenic diets have demonstrated some promising results when used with neurological diseases including MS.  Ketogenic diets have been used in the treatment of epilepsy since 500 B.C. and in the treatment of obesity since 1860.  It is now becoming apparent that ketogenic diets may play a very significant role in the treatment of neurological disease because of two-fold effects that arise when ketones become the primary fuel for the body.

First, when a person becomes keto-adapted and ketones are used as the primary fuel, instead of glucose, the body up-regulates mitochondria to use the ketones for fuel. As the ketone level rises,  the need for glucose diminishes.   This provides the nerve cell an alternative fuel source if glucose metabolism is impaired. It also decreases the need and production of insulin, a known hormone heavily involved in stimulating inflammation and inflammatory responses.

The second effect of a ketogenic diet is this favorable effect on inflammation.  It has been demonstrated that a ketogenic diet decreases reactive oxygen species, increased production of superoxide dismutase and catalayse, all of which notably decrease the inflammatory effects of oxidative stress (9,10, 11).  A ketogenic diet also is well known to raise glutithione levels, another anti-oxidant that decreases inflammation and oxidative stress (12-16).  This same anti-inflammatory and keto-adaptation effect can be obtained from intermittent fasting.

To date, studies in patients with neurologic diseases like MS, Alzheimer’s disease using ketogenic diets have had positive results in memory, cognition and diminished inflammation with evidence of halting or reversing the chronic demyelination (17,18, 19).  Still somewhat theoretical, the evidence points to effective dietary treatment and prevention for multiple sclerosis and other degenerative neurological diseases like Alzheimer’s Disease.

KetoOS

References:

  1. J. M. Pearce, “Historical descriptions of multiple sclerosis,” European Neurology, vol. 1, no. 1, pp. 49–53, 2005.
  2. C.-A. Castellano, S. Nugent, N. Paquet et al., “Lower brain 18F-fluorodeoxyglucose uptake but normal 11C-acetoacetate metabolism in mild Alzheimer’s disease dementia,” Journal of Alzheimer’s Disease, vol. 43, no. 4, pp. 1343–1353, 2014.
  3. S. Nugent, S. Tremblay, K. W. Chen et al., “Brain glucose and acetoacetate metabolism: a comparison of young and older adults,” Neurobiology of Aging, vol. 35, no. 6, pp. 1386–1395, 2014.
  4. H. Lassmann, W. Brück, and C. F. Lucchinetti, “The immunopathology of multiple sclerosis: an overview,” Brain Pathology, vol. 17, no. 2, pp. 210–218, 2007.
  5. C. Confavreux and S. Vukusic, “Natural history of multiple sclerosis: a unifying concept,” Brain, vol. 129, no. 3, pp. 606–616, 2006.
  6. P. K. Stys, G. W. Zamponi, J. van Minnen, and J. J. G. Geurts, “Will the real multiple sclerosis please stand up?” Nature Reviews Neuroscience, vol. 13, no. 7, pp. 507–514, 2012.
  7. P. G. Nijland, I. Michailidou, M. E. Witte et al., “Cellular distribution of glucose and monocarboxylate transporters in human brain white matter and multiple sclerosis lesions,” Glia, vol. 62, no. 7, pp. 1125–1141, 2014.
  8. L. C. Costantini, L. J. Barr, J. L. Vogel, and S. T. Henderson, “Hypometabolism as a therapeutic target in Alzheimer’s disease,” BMC Neuroscience, vol. 9, supplement 2, article S16, 2008.
  9. P. G. Sullivan, J. E. Springer, E. D. Hall, and S. W. Scheff, “Mitochondrial uncoupling as a therapeutic target following neuronal injury,” Journal of Bioenergetics and Biomembranes, vol. 36, no. 4, pp. 353–356, 2004.
  10. P. G. Sullivan, N. A. Rippy, K. Dorenbos, R. C. Concepcion, A. K. Agarwal, and J. M. Rho, “The ketogenic diet increases mitochondrial uncoupling protein levels and activity,” Annals of Neurology, vol. 55, no. 4, pp. 576–580, 2004.
  11. T. Shimazu, M. D. Hirschey, J. Newman et al., “Suppression of oxidative stress by β-hydroxybutyrate, an endogenous histone deacetylase inhibitor,” Science, vol. 339, no. 6116, pp. 211–214, 2013.
  12. S. G. Jarrett, J. B. Milder, L.-P. Liang, and M. Patel, “The ketogenic diet increases mitochondrial glutathione levels,” Journal of Neurochemistry, vol. 106, no. 3, pp. 1044–1051, 2008.
  13. J. B. Milder, L.-P. Liang, and M. Patel, “Acute oxidative stress and systemic Nrf2 activation by the ketogenic diet,” Neurobiology of Disease, vol. 40, no. 1, pp. 238–244, 2010.
  14. N. Dupuis, N. Curatolo, J. F. Benoist, and S. Auvin, “Ketogenic diet exhibits anti-inflammatory properties,” Epilepsia, vol. 56, no. 7, pp. e95–e98, 2015.
  15. D. Y. Kim, J. Hao, R. Liu, G. Turner, F.-D. Shi, and J. M. Rho, “Inflammation-mediated memory dysfunction and effects of a ketogenic diet in a murine model of multiple sclerosis,” PLoS ONE, vol. 7, no. 5, Article ID e35476, 2012.
  16. Y.-H. Youm, K. Y. Nguyen, R. W. Grant et al., “The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome—mediated inflammatory disease,” Nature Medicine, vol. 21, no. 3, pp. 263–269, 2015.
  17. A. Ramm-Pettersen, K. O. Nakken, I. M. Skogseid et al., “Good outcome in patients with early dietary treatment of GLUT-1 deficiency syndrome: results from a retrospective Norwegian study,”Developmental Medicine and Child Neurology, vol. 55, no. 5, pp. 440–447, 2013.
  18. Y. Ito, H. Oguni, S. Ito, M. Oguni, and M. Osawa, “A modified Atkins diet is promising as a treatment for glucose transporter type 1 deficiency syndrome,” Developmental Medicine and Child Neurology, vol. 53, no. 7, pp. 658–663, 2011.
  19. M. Storoni and GT Plant, “The Therapeutic Potential of the Ketogenic Diet in Treating Progressive Multiple Sclerosis,” Multiple Sclerosis International, vol. 2015, Article ID 681289, 9 pages, 2015.

Definition of Insanity: Cutting Calories/Restricting Fat & Expecting Weight Loss

Have you been cutting your calories and reducing fat and exercising your brains out and still not seeing the needle on the scale move that much?  Persistently and repetitively performing an action that doesn’t produce the desired result is insanity.  Cutting calories and reducing fat while expecting weight loss is akin to pouring water in the gas tank of your car and expecting it to run smoothly. Why do we do it? Are the 53, 000, 000 people with health club and gym memberships this year really insane?

This evening on PeriScope we touch on fat phobic insanity  and the limiting step that actually turns weight gain on or off. (We knew about this in the 1960’s, we just ignored it.)

You can see tonight’s PeriScope with the rolling chat-box questions here at Katch.me/docmuscles.  Or, you can watch the video stream below:

The only way to successfully loose weight is to modify or turn off the mechanisms that stimulate fat storage.  For years we have been told that this was just a problem of thermodynamics, meaning the more calories you eat, the more calories you store. The solution was, thereby, eat less calories or exercise more, or both. We are taught in school that a 1 gram of carbohydrate contains 4 kcal, 1 gram of protein contains 4 kcal, and 1 gram of fat contains 9 kcal.

If you ascribe to the dogma that weight gain or loss is due to thermodynamics, then it’s easy to see that cutting out fat (the largest calorie containing macro-nutrient) would be the best way limit calories.  For the last 65 years, we as a society have been doing just that, cutting out fat, exercising more (with the idea of burning off more calories) and eating fewer calories.

What has this dogma done for us? It’s actually made us fatter! (1)

World Obesity Rates
Obesity Rates Around the World

Some may argue that we really aren’t eating fewer calories and exercising more. But most people I have seen in my office have tried and tried and tried and failed and failed and failed to loose weight with this methodology. In fact, the majority of my patients attempt caloric restriction, exercise and dieting multiple times each year with no success. The definition of insanity is “doing the same thing over and over and expecting a different result.”

Most of my patients are not insane, they recognize this and stop exercising and stop restricting calories . . . ’cause they realized, like I have, that it just doesn’t work!

If you’re one that is still preaching caloric restriction and cutting out fat, I refer you to the figure above and the definition of insanity . . . your straight-jacket is in the mail.

So, if reducing the calories in our diet and exercising more is not the mechanism for turning on and off the storage of fat, then what is?

Before I can explain this, it is very important that you appreciate the difference between triglycerides and free fatty acids.  These are the two forms of fat found in the human body, but they have dramatically different functions.  They are tied to how fat is oxidized and stored, and how carbohydrates are regulated.

Fat stored in the adipose cells (fat cells) Triglycerides-and-Glycerol1as well as the fat that is found in our food is found in the form of triglycerides. Each triglyceride molecule is made of a “glyceride” (glycerol backbone) and three fatty acids (hence the “tri”) that look like tails. Some of the fat in our adipose cells come from the food we eat, but interestingly, the rest comes from carbohydrates

(“What! Fat comes from sugar?! How can this be?!!“)

de novo lipogenesis
De Novo Lipogenesis

We all know that glucose derived from sugar is taken up by the cells from the blood stream and used for fuel, however, when too much glucose is in the blood stream or the blood sugar increases above the body’s comfort zone (60-100 ng/dl), the body stores the excess. The process is called de novo lipogenesis, occurring in the liver and in the fat cells themselves, fancy Latin words for “new fat.”  It occurs with up to 30% (possibly more if you just came from Krispy Kream) of the of the carbohydrates that we eat with each meal.  De novo lipogenesis speeds up as we increased the carbohydrate in our meal and slows down as we decrease the carbohydrate in our meal. We’ve known this for over 50 years, since it was published by Dr. Werthemier in the 1965 edition of the Handbook of Physiology (2).

While we know that fat from our diet and fat from our food is stored as triglyceride, it has to enter and exit the fat cell in the form of fatty acids.  They are called “free fatty acids” when they aren’t stuck together in a triglyceride.  In their unbound state, they can be burned as fuel for the body within the cells. I like to think of the free fatty acids as the body’s “diesel fuel” and of glucose as the body’s version of “unleaded fuel.”  The free fatty acids can easily slip in and out of the fat cell, but within the adipose cell, they are locked up as triglycerides and are too big to pass through the cell membranes.  Lipolysis is essentially unlocking the glycerol from the free fatty acids and allowing the free fatty acids to pass out of the fat cell. Triglycerides in the blood stream must also be broken down into fatty acids Insulin and Triglyceridesbefore they can be taken up into the fat cells. The reconstitution of the fatty acids with glycerol is called esterification. Interestingly, the process of lipolysis and esterification is going on continuously, and a ceaseless stream of free fatty acids are flowing in and out of the fat cells.  However, the flow of fatty acids in and out of the fat cells depends upon the level of glucose and insulin available. As glucose is burned for fuel (oxidized) in the liver or the fat cell, it produces glycerol phosphate. Glycerol phosphate provides the molecule necessary to bind the glycerol back to the free fatty acids. As carbohydrates are being used as fuel, it stimulates increased triglyceride formation both in the fat cell and in the liver, and the insulin produced by the pancreas stimulates the lipoprotein lipase molecule to increased uptake of the fatty acids into the fat cells (3).

So when carbohydrates increase in the diet, the flow of fat into the fat cell increases, and when carbohydrates are limited in the diet, the flow of fat out of the fat cells increases.

Summarizing the control mechanism for fat entering the fat cell:

  1. The Triglyceride/Fatty Acid cycle is controlled by the amount of glucose present in the fat cells (conversion to glycerol phosphate) and the amount of insulin in the blood stream regulating the flow of fatty acid into the fat cell
  2. Glucose/Fatty Acid cycle or “Randle Cycle” regulates the blood sugar at a healthy level.  If the blood glucose goes down, free fatty acids increase in the blood stream, insulin decreases, and glycogen is converted to glucose in the muscle and liver.

These two mechanisms ensure that there is always unleaded (glucose) or diesel fuel (free fatty acids) available for every one of the cells in the body. This provides the flexibility to use glucose in times of plenty, like summer time, and free fatty acids in times of famine or winter when external sources of glucose are unavailable.

The regulation of fat storage, then, is hormonal, not thermodynamic. Unfortunately, we’ve know this for over 65 years and ignored it.

We’ve ignored it for political reasons, but that’s for another blog post . . .

References:

1. James, W. J Intern Med, 2008, 263(4): 336-352

2. Wertheimer, E. “Introduction: A Perspective.” Handbook of Physiology. Renold & Cahill. 1965.

3. Taubs, G. “The Carbohydrate Hypothesis, II” Good Calorie, Bad Calorie. Random House, Inc. 2007, p 376-403.

Pre-, Post-Workout Meal on Ketosis. Is it Important?

Today’s Periscope was an exciting one.  Do you really need a pre- or post-workout shake or meal?  How much protein do you need?  What’s the difference between ketosis and ketoacidosis?  Is Dr. Nally a ketogenic cheerleader? Get your answers to these and many more questions asked by some wonderful viewers this evening on today’s PeriScope.

https://katch.me/embed/v/5def6bce-4f67-363a-b5f9-3bbec8a8aea2?sync=1

Be sure to check out Dr. Nally’s new podcast called “KetoTalk with Jimmy and the Doc” with the veteran podcaster Jimmy Moore on KetoTalk.com.  The first podcast will be available on December 31, 2015.  KetoTalk with Jimmy and the Doc will be available for download for free on iTunes.

Stay tuned . . . !

The 3 Weight Loss Necessities to Weathering the Holidays

What are the three things you need to successfully weather the holidays with your ketosis lifestyle? What does a raindeer on a motorcycle look like? How does insulin resistance effect kidney stones and gout? How do you get back on track if you fall off the ketosis wagon? These and many more questions are answered by Dr. Adam Nally on tonight’s PeriScope.

You can see the video stream including the comment roll here at katch.me/docmuscles.  Or you can watch the video below:

How Do You Know if You’re Insulin Resistant?

How do you know if you're insulin resistant? What questions need to be asked? What should your numbers be? And, many other great ketosis questions. Also, why does Dr. Nally look like he has dirt on his chin? See it here . . .

Read more

What Lab Testing Do You Need to Start Your Weight Loss Journey?

What laboratory testing is necessary when you start your weight loss journey on a Ketogenic, Low-Carbohydrate, Paleolithic or any other dietary changes?  Why do you need them and what are you looking for?  We discuss these questions and others on today’s PeriScope.  Lots of questions from around the world to day . . . this one lasted a bit longer than normal . . . 45 minutes to be specific.  But it’s a good one because of all of your fantastic questions!  You really don’t want to miss this one.

You can see the video below or watch the video combined with the rolling comments here on Katch.me/docmuscles.

A list of the labs that we discussed are listed below:

  • Fasting insulin with 100 gram 2 or 3 hour glucose tolerance test with insulin assay every hour
  • CMP
  • CBC
  • HbA1c
  • Leptin
  • Adiponectin
  • C-Peptid
  • NMR Liprofile or Cardio IQ test
  • Lipid Panel
  • Urinalysis
  • Microalbumin
  • Apo B
  • C-reactive protein
  • TSH
  • Thyroid panel
  • Thyroid antibodies
  • AM Cortisol

This list will at least get one started, provide the screening necessary to identify insulin resistance (Diabetes In-Situ), Impaired fasting glucose, diabetes and allow for screening for a number of the less common causes of obesity.

I would highly recommend that you get these through your physician’s office so that appropriate follow up can be completed.  These labs will need to be interpreted by your physician, someone who understands and is familiar with various causes of obesity.

Until next time . . .

 

The Ketogenic Antidote to Chronic Renal Disease

It is well know that one of the most profound complications of diabetes is damage to the kidney and the very small arteries within the kidney acting as your body’s filtration system.  The kidney begins to lose the ability to adequately filter and retain microscopic protein progressively over time. As the blood sugar and insulin levels continually rise over time in the patient with diabetes or pre-diabetes, damage to the delicate filtering system of the kidneys occur. This very common and progressively damaging problem is called “nephropathy.”

nephropathy kidney
Chronic elevated blood sugar and insulin cause the filtering system to become more and more “leaky” and ineffective.

We knew in 1972 that patients with diabetes had thickening of the basement membrane or endothelium of the small tubles within the kidneys.  In fact, 98.6% of diabetics tested had thickening of this area of endothelium and tubules also called the renal glomeruli (1).  This allows the glomerulus or filtration system of the kidney to become more “leaky” and microscopic protein loss begins to occur through the kidney.  This loss of important proteins in the blood is called “albuminuria” or “micro-albuminuria.”  It is a flag that further damage of the kidney can and will occur without making significant changes to lower the blood sugar and the insulin. As of today, it is not totally clear how the basement membrane is damaged at the microscopic level, however, there is some evidence that elevated insulin has both a physical and immune type effect that stimulates oxidative stress, atherogenesis, immunoglobulins, as well as the formation advanced glycation end products leading to endothelial wall damage (2).

Recent research reveals that a ketogenic diet effectively repairs and/or completely reverses the albuminuria (3).

Evidence in my office of the significant improvement in micro-albumin can be seen in the one of a number of case studies below:

72 year old male with history of diabetes, diabetic nephropathy already treated with full dose statins, ACE inhibtors, metformin, and Januvia.  (Remember, microalbumin should be <30 mg/g)
Date                 Microalbumin      HbA1c
8/12/2010        2264 mg/g              6.4%   Started carb restriction <30 g per day.
10/01/2010        1274 mg/g               5.2%
1/08/2011            1198                          5.8%   Admits to cheating over holidays
12/26/2013         2434 mg/g            6.8%   Returned from 2 yr travel-off diet
2/27/2014          399 mg/g               6.3%  Restarted carb restriction <20g per day
6/20/2014           190 mg/g              7.0%  Traveling – no carb restriction
10/31/2014          280 mg/g              6.9%  Partial carb restriction <10 g/meal
3/14/2015            97 mg/g                6.8%

The patient began following a ketogenic diet in 2010.  After improvement he moved out of town for two years and “fell of the wagon.” Upon returning h restarted his carbohydrate diet and was only partially following it.  As you can see, he also admitted to some cheating on the carbohydrate restriction over the holidays.  In light of this, carbohydrate restriction decreased his albuminuria from 2400 to 97 mg/g within a period of 18 months.

References:

  1. Siperstein MS, Unger RH, Madison LL. “Further Electron Microscopic Studies of Diabetic Microagniopathy.” Early Diabetes: Advances in Metabolic Disorders, sup 1. New York: Academic Press, 1972, p261-271.
  2. Nasr SH, D’Agati VD.  “Nodular glomerulosclerosis in the nondiabetic smoker.”  J Am Soc Nephrol. 2007;18(7):2032.
  3. Poplawski MM, Mastaitis JW, Isoda F, Grosjean F, Zheng F, Mobbs CV (2011) Reversal of Diabetic Nephropathy by a Ketogenic Diet. PLoS ONE 6(4): e18604. doi:10.1371/journal.pone.0018604

Chewing the Phat with Dr. Nally (The Psychology of Fat & Many Other Questions)

Join me as we chew the phat of ketogenic lifestyles PeriScope style and answer many questions like, “Why do I get ‘hangry’?”  What causes hypoglycemia?  How many times a day should I eat? and many more . . .

We talk briefly about why 60% of people with insulin resistance may need methylated folic acid to help with B vitamin absorption/use and where it can be found.  (See me recent article about this called The Power of a Good Vitamin.)

You can see the whole PeriScope conversation on Katch.me/docmuscles with the comments scrolling or you can see the video stream below:

Thanks for visiting!!!

Fructose and High Triglycerides Lead to Leptin Resistance

I can’t help myself.  Some days I enjoy a good murder mystery, but on others, I enjoy a good journal article elucidating our understanding of leptin.  No, leptin is not a tiny Irish folk character or even a superhero. Leptin is a hormone.  It’s made by fat cells. Anything made by fat cells becomes fascinating to a “fat doctor.”

Why is learning about leptin illuminating?

Well, if Sir Arthur Conan Doyle was an Obesity Specialist, the mystery would have been that Mr. Plump was killed by the wrench in the kitchen, but the wrench seems to have never left tool case in the garage.  No one has been able to figure out how leptin, the allegorical wrench, plays its roll in lepin resistance.  We know that a lack of leptin allows hunger to persist and a person without leptin will continue to eat without the sensation of feeling full – leading to obesity.  What we haven’t understood is – what causes the brain to no longer sense larger and larger amounts of leptin being produced by those who are obese.

That is . . . we haven’t understood it until now. . .

We have known for some time that the hormone leptin is a key hormone produced by the adipose (fat) cells that suppresses hunger.  A majority of obese patients in my clinic have elevated circulating leptin levels 2-10 times the normal levels. We know that a lack of leptin leads to obesity, but the patients that I see in the office are producing an over abundance consistent with leptin resistance. The leptin signal is not being recognized by the brain.  This is very similar to type II diabetes and insulin resistance. The pancreas is producing an over abundance of insulin, but the cells are recognizing the signal to let the glucose in through the door way.

CNS Neural Pathways

Three recent and very interesting studies have pointed to the probable cause.  First, one of the most common genetic disorders causing human obesity is loss of function of the melanocortin receptor.

Leptin Effect on Hypothalamus
Image adapted from 2011 “The Skinny About Fat” presentation – Adam Nally, D.O.

If the MC-4R receptor is broken, suppression of appetite is limited, continued eating occurs and weight gain continues.  Leptin, produced by every adipose cell in the body, is carried in the blood stream to the brain and must pass through the blood-brain barrier.  Once it crosses the blood-brain barrier and enters the hypothalamus, it has a stimulatory effect on the MC-3R receptor in the Arcuate Nucleus of the hypothalamus causing stimulation of the MC-4R receptor in the Parventricular Nucleus and Lateral Hypothalamus to turn off hunger.

Most Common Obesity Genetic Disorder
Image adapted from 2011 “The Skinny About Fat” presentation – Adam Nally, D.O.

However, if leptin cannot cross the blood brain barrier, the signal is never received from the adipose cells and continued eating without satiation (feeling full) persists.  Studies have shown that dietary fructose ingestion alone or in combination with diets high in fat suppress the transmission of leptin across the blood-brain barrier.

Leptin resistance causes
Image adapted from 2011 “The Skinny About Fat” presentation – Adam Nally, D.O.

Fructose is the primary component of high-fructose corn syrup, and makes up 45-50% of every other type of natural form of sugar (sucrose).  Yes, it’s the major component found in table sugar, brown sugar, honey, agave, molasses and maple syrup.  This is why a Paleolithic Diet isn’t fully effective for people with leptin resistance.

sucrose

Lastly, anything that raises triglycerides inhibits leptin from crossing the blood-brain barrier.

Triglyceride effect on Leptin
Image adapted from 2011 “The Skinny About Fat” presentation – Adam Nally, D.O.

Insulin has a direct effect on triglycerides.  (See the articles “Insulin Resistance & The Horse,” “Fat Thoughts on Cholesterol,” “Ketogenic Living” and “So, What is this Ketogenic Thing?“).  If your insulin levels go up, triglyceride production goes up. The patient with insulin resistance, pre-diabetes, impaired fasting glucose or type II diabetes produces between two to ten times the normal amount of insulin when eating the standard American diet (SAD diet).  These patients have significant triglyceride elevation because of the high insulin response to carbohydrates in their diet.  (Many of them were told by their doctor that “It’s just genetic so take your Lipitor.”)  Statin drugs lower the LDL-C (calculated “bad cholesterol” level), but don’t reduce triglycerides effectively. Inadequate treatment of high triglycerides allows poor blood-brain barrier transmission of leptin and worsening leptin resistance.

In fact, this is the challenge and problem with the “frequent fasting” or “intermittent fasting” fad for weight loss that has been popping up in the blogosphere.  If fasting reaches a state of starvation (which is a very fine line metabolically), it stimulates a stress response . . . causing a spike in cortisol, release of glycogen (a form of sugar), a compensatory release of insulin and a spike in triglycerides.  If you have tried intermittent fasting and you’ve gained weight, you are probably not “fasting,” your probably “starving.” We’ve known for years that triglycerides are elevated in starvation.  This diminishes leptin’s ability to cross the blood-brain barrier and leads to worsening leptin and insulin resistance.

High leptin levels caused by leptin resistance also seems to play a significant role in the development of diabetic retinopathy – damage to the tiny blood vessels at the back of the eye feeding the retina.  Diabetic retinopathy starts insidiously without any symptoms initially and can lead to eventual blindness if not treated.  Leptin seems to upregulate vascular endothelial growth factor (VEGF) which leads to narrowing of the blood vessels called “ischemia.” Chronic ischemia of the retinal vessels leads to damage to the delicate retinal cells of the eye.

So what do you do if you have leptin resistance.  First, eliminate carbohydrates from your diet, especially sugars, high fructose corn syrup and any other form of simple sugar.  This is why I am such a big fan of low carbohydrate, high fat diets.

Second, lower your triglycerides. This is done through decreasing overall insulin loads and is very effectively accomplished with a ketogenic diet. You can find this in my book, The KetoCure.  Some additional great sources are KetoClarity, The Art and Science of Low Carbohydrate Living, and The Ketogenic Cookbook.

Third, use a supplement containing alpha-lipoic acid, carnosine high gamma vitamin E and benfothiamin (derivative of Vitamin B1).  These have been demonstrated to decrease inflammation and render protection to the blood vessels.

The use of Epigallocatechin gallate (EGCg), a derivative extract of green tea, has been shown to repress hepatic glucose production, one of the insidious factors of insulin resistance, and may play a role in stabilizing the effect insulin has on production of triglycerides. You should consider using KetoEssentials. It is my specially formulated multivitamin that contains all of the above supplements, and includes methylated folic acid (B9), the necessary vitamin B6 & B12, chromium, vandium & zinc that help to further stabilize insulin resistance.

Fourth, get a good night’s sleep.  Lack of sleep causes a stress response, increases cortisol, raises blood sugar and insulin leading to further leptin resistance.

Fifth, mild to moderate resistance exercise has been shown for years to improve insulin resistance significantly.  If you’re not exercising, take a 20 minute walk 2-3 times per week, ride a bike for 20 minutes, start a weight lifting program, consider yoga or Pilates,  Remember, jumping to conclusions, flying off the handle, carrying things too far, dodging responsibility and pushing your luck don’t qualify as resistance exercise.

Above all, if you’re having trouble losing weight, controlling insulin or leptin, see your doctor.  He or she can really help.

References:

  1. Ray F. Gariano, Anjali K. Nath, Donald J. D’Amico, Thomas Lee, and M. Rocio Sierra–Honigmann. “Elevation of Vitreous Leptin in Diabetic Retinopathy and Retinal Detachment.” Invest Ophthalmol Vis Sci. 2000;41:3576–3581
  2. Hammes HP, Du X . “Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy.” Nat Med. 2003 Mar;9(3):294-9. Epub 2003 Feb 18.
  3. Hipkiss AR, Brownson . “Reaction of carnosine with aged proteins: another protective process?” Ann N Y Acad Sci. 2002 Apr;959:285-94.
  4. Zachary A. Knight, K. Schot Hannan, Matthew L. Greenberg, Jeffrey M. Friedman. “Hyperleptinemia Is Required for the Development of Leptin Resistance.” PLoS ONE 5(6): e11376. doi:10.1371/journal.pone.0011376.
  5. Min-Diane Li. “Leptin and Beyond: An Odyssey to the Central Control of Body Weight.” The Yale Journal of Biology and Medicine. 2011;84(1):1-7.
  6. Eri Suganami, Hitoshi Takagi,Hirokazu Ohashi, Kiyoshi Suzuma, Izumi Suzuma, Hideyasu Oh, Daisuke Watanabe, Tomonari Ojimi, Takayoshi Suganami, Yasushi Fujio, Kazuwa Nakao, Yoshihiro Ogawa and Nagahisa Yoshimura. “Leptin Stimulates Ischemia-Induced Retinal Neovascularization: Possible Role of Vascular Endothelial Growth Factor Expressed in Retinal Endothelial Cells.” Diabetes. September, 2004. vol. 53 no. 9 2443-2448
  7. Joseph R. Vasselli, Philip J. Scarpace, Ruth B. S. Harris, and William A. Banks. “Dietary Components in the Development of Leptin Resistance.” Adv. Nutr. 2013: 4: 164–175.
  8. Joseph R. Vasselli. “Fructose-induced leptin resistance: discovery of an unsuspected form of the phenomenon and its significance.” Am J Physiol Regul Integr Comp Physiol. 2008 Nov;295(5):R1365-9. doi: 10.1152/ajpregu.90674.2008. Epub 2008 Sep 10.
  9. Waltner-Law ME, Wang XL Epigallocatechin gallate, a constituent of green tea, represses hepatic glucose production. J Biol Chem. 2002 Sep 20;277(38):34933-40. Epub 2002 Jul 12.

Lily's Chocolate . . . It's Quite Tastey!!

We just got a sample pack of Lily’s Chocolate.  This is a Stevia and erythritol sweetened chocolate that has no aftertaste and doesn’t cause the stomach upset that many experience with chicory root based products.  I am always looking for good low carbohydrate alternatives for snacks, as rescue foods, or to assist in baking.

My wife found this chocolate in a recipe that Carolyn Ketchum had posted on her website, All Day I Dream About Food.  It is quite tastey!! Thanks, Caroyln!! (By the way, I dream about food all day long, too.)

I scanned a copy of the wrapper for the Salted Almond & Milk Flavor.  I have to admit, I ate half the bar. It was that good!!

Lilys Stevia Sweetened Chocolate

For those looking for an alternative chocolate for a snack or to use in a recipe, this may be the answer.  You can find their whole line of chocolates here.

Hope this helps.

Don't Fear Fat

Dont Fear Fat

 

Don’t fear the fat.  If you haven’t seen the movie Cereal Killers, you should watch it by clicking here.   D.J. O’Neill ditches wheat and sugar in a food plan consisting of 70% fat – under the guidance of legendary South African Sports Scientist Prof. Tim Noakes.

The Obesity Paradox: The Intersection Where Agricultural Policy Contradicts Health Policy

Intent

The intent of this brief is to analyze the burden of obesity in the United States and to recommend policy changes to reduce the medical costs of obesity imposed upon the individual and country as a whole.

Introduction

Conventional fat reduction/caloric restriction guidelines for the treatment of obesity and associated cardiovascular disease, diabetes, cancer, and hypertension have been recommended since the early 1970’s.  Because these guidelines are based on questionable evidence, the cost of obesity has dramatically risen to almost 21% of overall health care costs in the United States (1).  This brief will analyze the current medical cost of obesity and will explain why the current obesity reduction guidelines perpetuate the problem. In addition, the brief will examine the impact of government agricultural policy on dietary habits, and will recommend changes to farm subsidy legislation in order to reduce the incidence of obesity and decrease costs to the healthcare system.

History & Background

The Cost of Obesity on the Nation

Obesity CostsAs of 2012, obesity accounts for nearly 21% of overall health care costs in the United States.  An obese person incurs $2741 more in medical expenses per year than his or her non-obese counterpart (1).  Medicare spending has increased per person per year by $600 for each obese beneficiary (includes out-patient and prescription drugs) and Medicaid beneficiary prescription drug spending increased by $230 per year per obese person. Private insurance has increased by $248 for prescription drugs and $443 for in-patient services for each obese beneficiary per year (2). That adds up to $190.2 billion spent annually on obesity-related medical problems (3).  This is a drastic change. Health care costs related to obesity were $85.7 billion (9.1% of overall health care costs) in 2006 and $61.2 billion (6.5%  of overall health care costs) in 1998 (4).

Obesity Prevalance 2011The most recent Center for Disease Control statistics reveal that 35.7% of the U.S. adult population is currently obese and another 33% is overweight.  Over 78 million adults and 12.5 million children are obese (5). The addition of 30 million people to the health care roles (current estimation of the Affordable Care Act including Medicaid expansion) means that an estimated $27 billion (in 2012 dollars) more will be spent per year on obesity-related health care costs.

Impact of Government Policy on Consumption

The ‘Farm Bill’ was originally enacted as part of President Franklin D. Roosevelt’s Agricultural Adjustment Act of 1933, which provided subsidies to American farmers in the midst of the Great Depression. Since that time the federal government has paid farmers not to grow seven specific crops – known as commodities – with the intent of decreasing the supply, increasing the demand, and thereby raising the price (7).  Dr. Susan Blumenthal, former Assistant Surgeon General and current SNAP to Health project director, writes, “The Farm Bill has since expanded to include many different categories or ‘titles.’ The last bill to be authorized, in 2008, had 15 titles, including nutrition (food stamps), crop subsidies, conservation, livestock, crop insurance and disaster assistance. The 2008 Farm Bill approved $300 billion in spending: 67% was spent on food stamps; 15% on agricultural subsidies; 9% on conservation; and 8% on crop insurance” (8).

The U.S. Department of Agriculture (USDA) Subsidy Programs tend to favor, either directly or indirectly, foods that increase obesity and other diseases. These subsidies support commodity crops, specialty crops, dairy products, livestock, and federal purchase programs.  Their justification is that they help to stabilize prices in agricultural commodity markets by balancing supply and demand (9).  Between 1995 and 2011, $277.3 billion were given in farm subsidies to almost 40% of U.S. farmers.  Arizona received $1.1 billion (mainly for cotton); however, only 7% of Arizona farms received subsides during this period (10).  These subsidies are incentives to grow and produce specific commodities that have a higher monetary return.  Subsidies also act as a disincentive for farmers to grow fruits and vegetables which fall under the “specialty crops” category.  This restricts both small and large farmers from diversifying their crops, and limits fruit and vegetable production (11).

Arizona farms received $25.3 million in dairy subsidies from 1995-2011 and $29.5 million in livestock subsidies during that same period (9).  Arizona ranks 2nd nationally in its production of cantaloupe & honeydew melons, head & leaf lettuce, spinach, broccoli, cauliflower and lemons, all of which are “specialty crops” and do not receive subsidies (12).  The most recent statistics show that the top five states receiving subsidies are Iowa, Texas, Illinois, Nebraska and Minnesota, with Kansas coming in at a close sixth.  The majority of these subsidies are for corn ($81.7 billion), soybeans ($26.4 billion), rice ($13.3 billion) and wheat ($34.4 billion) from 1995-2011 (10).  It is important to note that the Renewable Fuel Standard of 2012 (legislation protecting the corn-ethanol lobby) mandates that 37% of the corn harvest be used in ethanol production (13).

The food subsidies above have been in place since the Food, Conservation & Energy Act of 2002 and renewed in 2008.  They were only to be available for a period of five additional years and were set to expire September 30, 2012.  However, the American Taxpayer Relief Act of 2012 (H.R. 8), enacted by Congress and signed into law by President Barack Obama, included provisions that extended these subsidies until September 30, 2013 (20).

For many low-income Americans and especially children, federal programs have a direct and significant influence on food choices.  Subsidies where the money goesOver 30 million children receive government subsidized school lunch through National School Lunch Program (NSLP) administered by the USDA Food and Nutrition Service (14).  USDA-purchased meats, dairy products, grains, fruits, and vegetables are supplied to schools for use in meal programs.  Current school lunch recommendations on calorie intake set by the USDA and The Healthy, Hunger-Free Kids Act of 2010mandate school lunches provide 650-850 calories per meal to the 30 million children currently enrolled in this program (15).  Interestingly, that is the same caloric count of a Big Mac®, small fry and Diet Coke® from McDonalds® (16).  The rational for these purchase decisions are based upon agricultural support goals and adherence to national dietary guidelines (14).  A study published in the journal Economics and Human Biology reveals that a person’s body mass index (BMI) increased faster if that personwere on food stamps, and the BMI increased at a faster rate while on the Supplemental Nutrition Assistance Program (SNAP).  “We can’t prove that the Food Stamp Program causes weight gain, but this study suggests a strong linkage,” said Jay Zagorsky,  co-author of the study and a research scientist at Ohio State University’s Center for Human Resource Research (17).  However, much of the food available through the SNAP programs are refined, subsidized high-carbohydrate containing foods.

The price of food influences an individual’s consumption choices (6).  Foods that are refined contain increased amounts of sugar or high-fructose corn syrup. These foods contain more caloric density and are often cheaper and more easily accessible.  These are foods that are usually found in the center of the grocery store and frequently on sale at the end-caps of each isle.  Nutrient-dense, higher fiber foods are frequently associated with higher prices and are consumed less often.  These are the foods you usually find around the peripheral areas of the grocery store (fruits, vegetables, etc.)  Current food subsidy policy found in the Food, Conservation and Energy Act of 2008 extension mandated by the American Taxpayer Relief Act of 2012 drives up the price of fruits, vegetables, and meats. This policy also turns people toward lower cost foods that are higher in simple carbohydrates and caloric density.  Thus, current policy is actually making obesity worse and making America fatter.  Research completed at the University of Illinois at Chicago reveals that small taxes or price changes do not produce a change in a person’s BMI; however, more significant price change has a measurable and significant effect on weight in both adults and children.  Price increases of 100-150% have been shown to change purchasing behavior and thereby affect health (18).  An example of this is the tax levied on cigarette smoking.

The USDA disagrees with the amount of influence they have over the individual American’s food choices.  They state openly on their website that “Some public health advocates have argued that falling real, or inflation-adjusted, prices for many high-calorie foods encourage people to buy and consume more of these foods, leading to poor diet quality and rising rates of obesity. A closer look at how consumers respond to food price variation–over time, across geographic markets, in different types of stores, and in response to taxes and subsidies–reveals how food prices affect people’s food choices, and their waistlines. In short, price matters, but not very much, and it is not the only factor” (19).

Why Current Dietary Guidelines Have Not Been Effective

Why do we get fat?  Why have we not been successful in losing weight via diet and exercise? The obesity paradox was described by Jules Hirsch of Rockefeller University, who proposed two opposing hypotheses:

 

  1. “Obesity is the result of a willful descent into self-gratification” implying that we gain weight because we over-eat (caloric excess) leading to caloric imbalance.
  2. “Alternative hypothesis is that there is something ‘biologic’ about obesity, some alteration of hormones, enzymes or other biochemical control systems which leads to obesity” (22).

The 1977 Dietary Goals for the United States – the first comprehensive statement by any branch of the federal government about the American diet – supported the first theory. The Guidelines were heavily influenced by the American Heart Association’s position that fat intake alone would cause heart disease. The USDA 2011 Dietary Guidelines imply that the “people who are the most successful at achieving and maintaining a healthy weight do so through continued attention to consuming only enough calories from foods and beverages to meet their needs and by being physically active.” (15)

Current research contradicts the caloric restriction or “calorie in – calorie out” theory.  Scientific evidence clearly demonstrates the domino effect of carbohydrate or starch intake increasing insulin levels which thereby stimulates obesity by raising cholesterol and triglyceride levels. Time Magazine recently published evidence that the longstanding recommendations to “eat less high-fat red meat, eggs and dairy and replace them with more calories from fruits, vegetables and especially carbohydrates” is now seen as incorrect (45).  Even our medical textbooks from 1965, like the introductory chapter of the Handbook of Physiology, make it clear that carbohydrate intake cause weight gain and raise triglyceride and cholesterol levels (22), (23), (24).

Current Policy

The current version of the Farm Bill was set to expire September 30th, 2013.  If it had been allowed to expire, the results would have returned us to the 1949 Farm Bill legislation and theoretically double the price of milk. However, this would have had the effect of freeing up over $5 billion dollars of federal spending per year and would also lead to decreased consumption of a major source of carbohydrates in the standard American diet like wheat and corn.  Senator Debbie Stabenow (D-MI), and chairwoman of the Senate Agriculture Committee, had repeatedly said she was opposed to an extension; however, she agreed to a compromise extending the bill for another year to help the farmers experiencing serious drought conditions in 2012 (7).  Two additional extensions were passed in the House and Senate, but because these differed so significantly, it was referred to a House-Senate Conference Committee to work out the compromise details.  With only $23 billion in spending reductions, The Agricultural Act of 2014 was passed on January 29, 2014 (46).   

Outcomes and Stakeholders

Obesity Trends 1960-2008If the United States continues its current course, up to 58% of the population will be obese by 2030 (26).  Many believe that the USDA Dietary Guidelines are to blame.  Richard David Feinman, President of the Nutrition and Metabolism Society and Professor of Cell Biology at SUNY Downstate Medical Center said, “The previous Guidelines have not worked well.  It is unreasonable to ask the Dietary Guidelines Advisory Committee (DGAC) to audit its own work.  An external panel of scientists with no direct ties to nutritional policy would be able to do a more impartial evaluation of the data.  This would be far better for everyone.” (27) A recent Gallup Poll reveals that 63% of Americans believe the USDA Guidelines that a low fat, calorie restricted diet will help in reduction of obesity, and the same study showed that 48% of Americans worry about their weight “all of the time or some of the time” (28).  Recent evidence from the Women’s Health Initiative Dietary Modification Trial studying 49,000 women supports Dr. Feinman’s conclusion above. It did not show any statistically significant evidence that following a low-fat or caloric restricted diet had any effect upon obesity (29). Other nutritional experts from the Salt Institute and the National Health Coalition have expressed their support for significant changes to the USDA Dietary Guidelines (30).  The Weston A. Price Foundation, which according to its website is “dedicated to restoring nutrient-dense foods to the human diet through education, research and activism,” also supports the view that the current USDA Dietary Guidelines have been a significant cause of obesity and have been an active voice promoting legislative change (31).

On the other hand, the Sugar Association has issued statements that sugar is not the cause of obesity and “continually eating too much food and sedentary lifestyles are the major contributing factors to increasing rates of obesity – not sugar intake” (32).  In addition, the American Beverage Association has stated that sugars are not the problem with obesity, but instead, “overweight and obesity are a result of an imbalance between calories consumed and calories burned” (33).

Attempts at modifying the Farm Bill with legislation like the 2012 DeMint Amendment (SA 2276 ) were supported by both Arizona Senators McCain (R-AZ) and Kyl (R-AZ) with a “Yes” vote, as well as Senators Ayotte (R-NH), Brown (R-MA), Burr (R-NC), Coats (R-IN), Coburn (ROK), Cornyn (R-TX), DeMint (R-SC), Graham (R-SC), Hatch (R-UT), Heller (R-NV), Johnson (R-WI), Lee (R-UT), McConnell (R-KY), Murkowski (R-AK), Paul (R-KY), Rubio (R-FL), Sessions (R-AL), and Toomey (R-PA).  However, because of a large lobbying agricultural coalition, it was voted down (34).  Changing farm subsidies will be a great challenge as 40% of the farmers in the U.S. now have some degree of dependence upon these subsidies.  The following agricultural groups have historically had significant monetary interest in the farm subsidies that these amendments would affect:

  • American Beekeeping Federation
  • American Farm Bureau Federation American Mushroom Institute
  • American Sheep Industry Association American Soybean Association
  • National Cattlemen’s Beef Association National Corn Growers Association National Cotton Council
  • National Council of Farmer Cooperatives National Farmers Union
  • National Milk Producers Federation National Pork Producers Council
  • National Potato Council
  • National Sorghum Producers
  • National Watermelon Association
  • Produce Marketing Association
  • United Dairymen of Arizona
  • United Egg Producers
  • United Fresh Produce Association
  • Western Peanut Growers Association

The following groups have formed coalitions in support of the Farm Bill: Health/Food Justice/Farm Group partnerships, Specialty Crop Farm Bill Alliance, Community Food Security Coalition, Center for a Livable Future at Johns Hopkins University, Collaboration for a Healthy Sustainable Food System, and the Healthy Farms, Healthy People: A Farm & Food Policy Summit for a Strong America.

The American Heart Association’s position is that the Farm Bill needs to be modified to include increased access to fruits and vegetables (35).  The American Medical Association’s position in 2008 and 2011 has been for cutting the size and budget of the current Farm Bill (36).  The American Osteopathic Association does not currently have a formal position on the Farm Bill.

If certain crops like corn or wheat were no longer subsidized,drastic changes will be likely in the food manufacturing industry, which would likely be the largest proponent against change.  Unintended consequences of modifying the Farm Bill and not extending its subsidies could have the short term effect of escalating the price of a number of commodities to two to three times their current price.  For example, the price of milk would increase to $6-$8 dollars a gallon without federal subsidies (37).  This would likely deter the use of carbohydrates containing dairy products, but may also increase the price of meats and cheeses as well.

The USDA’s Rural Development Progress Report claims that the subsidies it distributed “saved more than 75,000 jobs” in 2006 and over 400,000 jobs in 2011 (38), (39). They claim that without federal farm subsidiesthere would be significant loss of jobs; however, studies from the Cato Institute actually show the opposite.

“Job gains are weak and population growth is actually negative in most of the counties where farm payments are the biggest share of income. Job growth is decidedly weak in the counties most dependent on farm payments. The vast majority of such counties (483) had job gains below the 19 percent national average from 1992 to 2002. A considerable number (167) had outright job losses over the period. In short, farm payments are not yielding robust economic and population gains in the counties where they should have the greatest impact. If anything, the payments appear to be linked with sub-par economic and population growth. To be sure, this quick comparison cannot answer whether growth would have been even weaker in the absence of the payments.  Still, farm payments appear to create dependency on even more payments, not new engines of growth” (40).

As of 2010, obesity costs about $73.1 billion per year in lost productivity in the United States (43).  The worsening obesity epidemic poses further workforce productivity losses up to 20% more by 2030.  Even small improvements in obesity will improve workforce productivity and has substantial potential for savings.  Currently, the Affordable Care Act allows employers to charge obese employees 30-50% more for health insurance.  Without correcting this epidemic, it may be impossible for many to afford health care, opting out to pay the less expensive tax penalty. This would have the effect of increasing commercial premiums across the country, feasibly pushing private insurance companies out of business and forcing a single payer governmental system.

Recommendations

This brief points out that the overall U.S. healthcare costs associated with obesity have increased by 68% in the last fourteen years.  It provides evidence that using current dietary low-fat caloric restriction guidelines show poor statistically significant improvements in obesity.  And it provides evidence that obesity is not caused by excessive caloric intake and fat, but by insulin response to carbohydrate intake.  Lastly, this analysis provides evidence that the Farm Bill propagates continued worsening obesity rates in the US by providing access to cheap, fattening food.

The USDA 2011 Dietary Guidelines need to be revised to reflect current evidence-based obesity prevention and weight reduction research.  The guidelines should include information about limiting the intake of foods high in carbohydrates.

The food subsidy extension provided in the American Taxpayer Relief Act of 2012 was extended five years by the Agricultural Act of 2014.  Had it been allowed to expire, it would have saved the country over $200 billion over the next ten years.  However, because of so many entitlements involved in this bill, the House and Senate convened in Conference that resulted in a compromise of only $23 billion dollars in spending reductions, the first SNAP reforms since 1996 reducing waste, but did nothing in eliminating subsidies that drive or influence eating behavior (46).

When significant price changes occur, eating behavior will change.  As the price of fattening carbohydrates increases, people will eat less of them, leading to a national decrease in obesity and overweight.  The current reforms did nothing that will change our dietary behavior.

References

1. Cornell University. Obesity accounts for 21 percent of U.S. health care costs, study finds. Science Daily. [Online] April 9, 2012. [Cited: January 5, 2013.] http://www.sciencedaily.com/releases/2012/04/120409103247.htm.

2. Annual Medical Spending Attributable To Obesity: Payer-And Service-Specific Estimates. Eric A Finkelstein, Justin G Trogdon, Joel W Cohen and William Dietz. Health Affairs, 28, Bethesda, MD : Project HOPE, 2009, Vol. 5. 10.1377/hlthaff.28.5.w822.

3. Begley, Sharon. As America’s Waistline Expands, Costs Soar. Reuters. [Online] Thompson Reuters, April 30, 2012. [Cited: January 5, 2013.] http://www.reuters.com/article/2012/04/30/us-obesity-idUSBRE83T0C820120430.

4. Ungar, Rick. Obesity Now Cost Americans More In Healthcare Spending Than Smoking. Forbes. [Online] 4 30, 2012. [Cited: January 5, 2013.] http://www.forbes.com/sites/rickungar/2012/04/30/obesity-now-costs-americans-more-in-healthcare-costs-than-smoking/.

5. Ogden CL, Carroll MD, Kit BK, Flegal KM. Prevalence of obesity in the United States, 2009–2010. NCHS data brief, no 82. Hyattsville, MD : National Center for Health Statistics, 2012, 2012.

6. Poverty and Obesity: The Role of Energy Density and Energy Costs. A Drewnowski, SE Specter. s.l. : American Journal of Clinical Nutrition, 2004, Vols. 79:6-16.

7. Laprete, Jay. U.S. Farm Bill. Times Topics. [Online] The New York Times, December 31, 2012. [Cited: February 11, 2013.] http://topics.nytimes.com/top/reference/timestopics/subjects/f/farm_bill_us/index.html?offset=0&s=newest.

8. SNAP to Health. U.S. Farm Bill: Frequently Asked Questions. SNAP to Health. [Online] CSPC / Snap to Health, 2013. [Cited: February 11, 2013.] http://www.snaptohealth.org/farm-bill-usda/u-s-farm-bill-faq/.

9. USDA. Agricultural Marketing Service. Commodity Purchasing. [Online] January 22, 2013. [Cited: February 10, 2013.] http://www.ams.usda.gov/AMSv1.0/ams.fetchTemplateData.do?template=TemplateQ&navID=Commodity%20Purchasing%20Main%20Page&rightNav1=Commodity%20Purchasing%20Main%20Page&topNav=&leftNav=CommodityPurchasing&page=CommodityPurchasing&resultType=&acct=cmdtyprchs.

10. Environmental Working Group. United States Summary Information. EWG Farm Subsidies. [Online] 2012. [Cited: February 10, 2013.] http://farm.ewg.org/region.php?fips=00000.

11. Monke, Jim. Farm Commodity Programs: Base Acreage and Planting Flexibility. Washington, DC : Congressional Research Services, 2003.

12. Arizona Farm Bureau Federation. AG Facts. Arizona Farm Bureau. [Online] 2013. [Cited: February 15, 2013.] http://www.azfb.com/ag-facts.html.

13. Children of the Corn: The Renewable Fuels Disaster. The American. [Online] American Enterprise Institute, January 4, 2012. [Cited: February 15, 2013.] http://www.american.com/archive/2012/january/children-of-the-corn-the-renewable-fuels-disaster.

14. USDA Food & Nutrition Service. National School Lunch Program. USDA Food & Nutrition Serivce. [Online] June 21, 2012. [Cited: February 15, 2013.] http://www.fns.usda.gov/cnd/lunch/.

15. U.S. Department of Agriculture (USDA). USDA 2010 Dietary Guidelines. USDA Center for Nutrition Policy and Promotion: Dietary Guidelines for Americans. [Online] U.S. Government Printing Office, January 31, 2011. [Cited: January 5, 2013.] http://www.cnpp.usda.gov/Publications/DietaryGuidelines/2010/PolicyDoc/Chapter2.pdf.

16. ABC News. ABC News. Medical Unit. [Online] ABC News Internet Ventures, September 30, 2012. [Cited: April 14, 2013.] http://abcnews.go.com/blogs/health/2012/09/30/school-lunch-showdown-850-calorie-meals-compared/.

17. Ohio State University. Food Stamp Use Linked To Weight Gain, Study Finds. Science Daily. [Online] August 12, 2009. [Cited: April 13, 2013.] http://www.sciencedaily.com­ /releases/2009/08/090810122139.htm.

18. Food Prices and Obesity: Evidence and Policy Implications for Taxes and Subsidies. L Powell, F Chalupka. 1, Illinois : The Milbank Quarterly by Wiley Periodicals Inc, 2009, Vol. 87.

19. Jessica Todd, Biing-Hwan Lin. Amber Waves Online Magazine. U. S. Department of Agriculture Economic Research Service. [Online] September 2012. [Cited: February 10, 2013.] http://www.ers.usda.gov/amber-waves/2012-september/what-role-do-food-and-beverage-prices.aspx.

20. American Taxpayer Relief Act of 2012. U.S. Government Printing Office. [Online] Jan 12, 2012. [Cited: February 10, 2013.] http://www.gpo.gov/fdsys/pkg/BILLS-112hr8enr/pdf/BILLS-112hr8enr.pdf.

21. Bruch, Hilde. The Importance of Overweight. Michigan : Norton, University of Michigan, 1957.

22. Taubs, Gary. Good Calories, Bad Calories: Fats, Carbs, and the Controversial Science of Diet and Health. New York : Anchor Books, 2007. 978-1-40000-3346-1.

23. Role of Insulin in Endgenous Hypertriglyceridemia. GM Reave, RL Lerner, MP Stern, JW Farquhar. s.l. : Journal of Clinical Investigation, 1967, Vols. 46(II):1756-67.

24. High-Carb Diets Questioned. Kolata, G. 235(4785):164, s.l. : Science, 1987, Vol. 9.

25. U.S. Department of Health and Human Services. The Surgeon General’s Call to Action to Prevent and Decrease Overweight and Obesity. Washington, D.C. : U.S. Government Printing Office, 2001.

26. Global Burden of Obesity in 2005 and Projections to 2030. T Kelly, W Yang, C-S Chen, K Reynolds and J He. 8 July 2008, New Orleans : International Journal of Obesity, 2008, Vols. 32, 1431–1437. doi:10.1038/ijo.2008.102.

27. In The Face Of Contradictory Evidence: Report Of The Dietary Guidelines For Americans Committee. Adele H Hite, Richard D Feinman, Gabriel E Guzman, Morton Satin, Pamela Schoenfeld, Richard J Wood. 10, s.l. : Nutrition, 2010, Vol. 26. DOI: 10.1016/j.nut.2010.08.012.

28. A Dugan, F Newport. Gallup Wellbeing. Gallup. [Online] August 17, 2012. [Cited: April 13, 2013.] http://www.gallup.com/poll/156710/americans-say-low-fat-diet-better-low-car.aspx.

29. Low-fat dietary pattern and weight change over 7 years: the Women’s Health Initiative Dietary Modification Trial. . Howard BV, Manson JE, Stefanick ML, et al. s.l. : JAMA, 2006, Vols. 295:39-49. doi:10.1001/jama.295.1.39.

30. Healthy Nation Coalition. Healthy Nation Coalition. Healthy Nation Coalition. [Online] Adrienne Larocque, PhD, 2012. [Cited: March 8, 2013.] http://www.forahealthynation.org/.

31. Judith McGeary, Esq. Legislative Updates. The Weston A. Price Foundation. [Online] December 11, 2012. [Cited: March 9, 2013.] http://www.westonaprice.org/legislative-updates/policy-update-farm-bill-and-gmos.

32. The Sugar Association. Sugar and Your Diet. Sugar.org. [Online] 2012. [Cited: March 9, 2013.] http://www.sugar.org/sugar-and-your-diet/caloric-intake.html.

33. American Beverage Association. Obesity. American Beverage Association. [Online] 2013. [Cited: March 9, 2013.] http://www.ameribev.org/nutrition–science/obesity/.

34. Library of Congress. S.Amdt.2276 to S.3240. Congress.Gov. [Online] March 8, 2013. [Cited: March 9, 2013.] http://beta.congress.gov/amendment/112th-congress/senate-amendment/2276.

35. The American Heart Association. Policy Brief – The Farm Bill. The American Heart Association. [Online] 2012. [Cited: April 14, 2013.] http://www.heart.org/idc/groups/heart-public/@wcm/@adv/documents/downloadable/ucm_429110.pdf.

36. AMA: Report of Reference Committee . Malechek, Lindsay. 2011.

37. Wolf, Jim. Senate, House agriculture committees in deal to avert milk price spike. Reuters. Sun, Dec 30, 2012, 2012.

38. USDA. USDA Rural Progress Report. USDA. [Online] December 2006. [Cited: April 14, 2013.] http://www.rurdev.usda.gov/rd/pubs/2005_06_Prog_Report.pdf.

39. —. USDA Rural Developement 2011 Progress Report. USDA Rural Developement. [Online] December 2011. [Cited: April 14, 2013.] http://www.rurdev.usda.gov/Reports/RD%20Progress%20Report%202011–Smallest(2).pdf.

40. Slivinski, Stephen. Rural Subsidies. Cato Institute. [Online] July 2009. [Cited: March 9, 2013.] http://www.downsizinggovernment.org/agriculture/rural-subsidies.

41. Obesity prevention: the role of policies, laws and regulations. Swinburn, Boyd A. New Zeland : BioMed Central Ltd., 208, Vol. 5:12. 10.1186/1743-8462-5-12.

42. Begley, Sharon. As America’ss Waistline Expands, Costs Soar. Reuters. [Online] Thompson Reuters, April 30, 2012. [Cited: January 5, 2013.] http://www.reuters.com/article/2012/04/30/us-obesity-idUSBRE83T0C820120430.

43. The Costs of Obesity in the Workplace. E Finkelstein, M DiBonaventura, S Burgess, B Hale. 10, Illinois : Lippincott Williams & Wilkins, 2010, Vol. 52. doi: 10.1097/JOM.0b013e3181f274d2.

44. Rudd Center For Food Policy & Obesity. Search Legislation Database. Yale Rudd Center. [Online] Rudd Center, 2013. [Cited: January 5, 2013.] http://www.yaleruddcenter.org/legislation/search.aspx.

45. Walsh, Bryan. “Ending The War on Fat.” TIME Magazine. June 12, 2014.

46. Lucas, Frank D. “Agricultural Act Summary.” House Agricultural Committee. [Online]  Jan 29, 2014. [Cited June 28, 2014.] http:// http://agriculture.house.gov/farmbill

Insulin Resistance and The Horse

Adam and Bailey
Adam & Bailey in Bull Dog Canyon

As a family practice physician and bariatrician, my job is to examine and treat the “Diseases of Civilization.”  The Diseases of Civilization are those diseases arising out of the changes induced by industrializing and modernizing a society of people. These include diseases like diabetes, dyslipidemia (abnormal cholesterol), heart disease, hypertension, gout, vascular disease, & stroke. It is interesting that the so called Diseases of Civilization didn’t really appear on the scene until the early 1900’s. Yes, we have now identified some of these diseases in the early Egyptians, but to my point, as a society modernizes or industrializes, certain types of disease begin to arise. The Canadian cardiologist William Osler, one of the founding professors of John’s Hopkins Hospital, documented the first “syndrome” associated with narrowing of the arteries causing heart disease at the turn of the 19th century, and in 1912, the American Cardiologist James Herrick is credited with the discovery that narrowed arteries cause angina, a form of chest pain with exertion.

Today we know that underlying each of these diseases is the phenomenon of insulin over production, which seems to arise between five and twenty years prior to the onset of the Diseases of Civilization. Metabolic Syndrome, Dysmetabolic Syndrome or Syndrome X is the name we’ve given to the presentation of three or more of these diseases at once in one person. There is still argument as to whether insulin over production is the chicken or the egg, but what I see clinically has convinced me that insulin is culprit.

Insulin Resistance
May 2013 Metabolism “Insulin Resistance: An adaptive mechanism . . .” 62(5):622-33. doi: 10.1016/j.metabol.2012.11.004. Epub 2012 Dec 20.

Insulin is a very powerful hormone that acts as a key, opening a door in just about every cell in the body, letting glucose (the primary form of fuel derived from carbohydrate) into the cell.  For reasons that appear to be genetic,  this key becomes “dull” in a portion of the population and does not unlock the door fast enough to lower the blood sugar.  So, the body panics, and stimulates production of additional insulin, 2-10 times more in many people.  However, the insulin that was produced initially, eventually kicks in.  This extra insulin, acting at a slower rate, is the underlying culprit to the Diseases of Civilization.

How, you ask? Let me explain.

Insulin does more than just open the door for glucose.

1. Insulin causes weight gain. It turns on the storage of fat by activating an enzyme called lipoprotein lipase, pulling the triglycerides out of the cholesterol molecules and depositing them in the adipose tissue (fat cells).

2. Insulin raises cholesterol. It drives increased triglyceride production in the liver, especially in the presence of fructose.

3. Insulin triggers atherosclerosis. Triglycerides are essentially the passenger in the LDL (bad cholesterol) molecule.  Higher triglycerides cause increased LDL production leading to increased atherosclerosis (narrowing of the arteries).

4. Insulin causes gout & kidney stones. Insulin increases uric acid production and in a round about way can increase calcium oxylate as well, increasing the risk of kidney stones and gout.

5. Insulin raises blood pressure. Insulin stimulates the retention of sodium, causing and increase in blood pressure.

Tiffini and Jazz
Tiffini & Jazz riding near the top of the White Tank Mountains

6. Insulin makes inflammation worse. Insulin drives the inflammatory cascade and increases free radicals, and stimulates the inflammatory hormones causes arthritis, allergic rhinitis, psoriasis, dermatitis, and inflammatory bowel problems to be amplified.

My intent is not to demonize insulin. It is an essential hormone, however, when five to ten times the normal amount of insulin is being produced, you’re going to amplify the problems above by five to ten times normal.   Type II Diabetes is really just a consequence of 15-20 years of over production of insulin.

This isn’t just something that affects humans. either.  We have been seeing this in other species of the animal kingdom as well.  Take for example my wife’s horse, Jazz. She’s a beautiful grey Arab/Saddle-Bred who kept having problems with laminitis, or more colloquially known as “founder.” Her diet consisted predominantly of alfalfa at the time, considered a moderate starch containing form of feed.

Laminitis is a progressively increasing tenderness to the hoof of horses or cattle that can be disabling and if not treated appropriately can cause permanent lameness in the animal. Recent literature in the veterinary world have identified that animal diets high in starch have a propensity to cause laminitis as well as colic.  First identified in the equine community in the 1980’s with glucose tolerance tests, insulin resistance has been identified as a significant factor in hoof disease. The use of Corn, Oats, Barley or even Alfalfa as a primary form of feed for a horse with insulin resistance greatly increases the risk of laminitis.

Like Jazz, many horses in the arid Arizona climate are fed primarily with oats and alfalfa. Jazz was tested and found to have insulin resistance. Since Jazz has been placed on a much lower starch containing feed, she has had no further problems with laminitis.  We converted all our horses to Bermuda grass.

Horses in Pasture
Bailey, Jazz, Nayha & Houdini grazing in the back pasture

Our family and our horses are all now on Low-Carb diets to some degree and have been for the last seven years. No further hoof problems with the horses, and 55 lbs of weight loss with normalization of cholesterol in their owner, me.

Trail Ride White Tanks
Trail Riding in the White Tank Mountains

For those with interest, studies reveal feeds in order of the highest to lowest starch (carbohydrate) content to be: Sweet Feed, Corn, Oats, Barley, Wheat Bran, Beat Pulp, Alfalfa, Rice Bran, Soybean hulls, Bermuda Grass.  Take a look the Low Carbohydrate help section in the menu above to see the carbohydrate content of many of the foods for human consumption.

It’s time we recognize that our diet and lifestyles have lead us to the Diseases of Civilization, and those diets and lifestyles have even effected our animals.

 

Low Carb Cheese Cake

My amazing wife, among her many talents, makes a wonderful low carb cheese cake.  She has taken the recipe found in Maria Emmerich’s “Secret Weight Loss Recipes” and modified it to our family’s taste.  It has quickly become one of my family’s favorites.

Low Carb Cheesecake = 1 gram carb per serving
Individual spring-form serving pans
Crust:
2 cups almond flour
1/4 cup coconut flour
1/2 cup butter melted
Pinch of salt
1/2 cup erythritol
Mix and press into spring-form pan.
5 (8 oz) packages cream cheese, softened
1 cup erythritol and 1 tsp liquid Stevia
1 TBS vanilla
1/2 cup whey Protein
1 cup sour cream
3 eggs
Preheat oven to 350F. Mix cream cheese, sweetener, protein and vanilla with an electric mixer until blended. Add eggs one at a time, mixing on low after each until blended. Blend in sour cream and pour over crust. Place a pan of water on the lower rack place cheesecake on rack above. Bake for approximately 45 minutes until set. Watch carefully!
Refrigerate overnight.
Freezes well too!
My wife will often bake them in individual sized pans (as in the picture above) so that I can pull one out of the freezer, let it thaw and cover it in whip cream and a sprinkle of berries.  Tastes fantastic!
One serving is = 1 gram of carbohydrate.

How To Start Your Weight Loss Journey

Weight loss, better put as “fat loss,” is a journey.  A journey brought you to where you stand today, and it will be an even more exciting journey getting back to that size you’ve been daydreaming about.  So, how do you most effectively start down the path of this journey?
That is the great question.  It is the most important question I get asked every day.  In the words of Napoleon Hill, “Desire is the starting point of all achievement, not a hope, not a wish, but a keen pulsating desire which transcends everything.”

First, Know Where You Are Coming From.
A journey requires knowing where you were, were you are today and where you want to go.  Get a journal and weight yourself.  Write it down and then check your weight every 3-5 days.  DO NOT weigh yourself every day.  I repeat DO NOT weight yourself every day. This can be discouraging because is is normal to fluctuate 2-5 lbs every day based on meals and water intake.   Many people see this fluctuation and thing they are failing, then give up.  The journal helps this.  Recording your weight helps you see the progress.

The journal is also to help you record what you eat.  Plan and record your meals IN YOUR JOURNAL.  If you are being followed by a weight loss specialist, they will want to see your journal.  If you are seeing me in my office, bring the journal with you to EVERY visit.  Record every thing you eat.  PlanAnd, record your water intake.  I am amazed at how many of my patient’s are dehydrated and just putting water back into their systems help them loose weight.

Second, Plan Your Day.
Planning is the key to weight loss on any program.  
You should plan your exercise and plan your meals the night before.  Failing to plan is really just planning to fail.  Your plan should include 1) keeping carbohydrate intake less than 20 grams per day and 2) getting adequate proteins to match your goals. 

Third, What’s the Underlying Cause of Your Weight Struggles?

You can’t effectively lose weight unless you understand why you are gaining weight.  Two thirds of my patients are hyperinslinemic – they produce too much insulin in response to any sugar, starch or carbohydrate.  This is also called “insulin resistance.”  This is the primary cause of weight gain in 85% of the population.  People produce between two to thirty times the normal amount of insulin in response to a piece of bread or a bowl of cereal.   When they eat a single piece of bread, their bodies respond as if they ate the whole loaf.  If they eat a bowl of cereal, their bodies respond as if they ate the whole box of Captain Crunch.

This variable over production of insulin is why some patient’s gain more weight than others eating and exercising the same way.  Your doctor can easily identify this through blood work.  For starters, if your waist circumference is larger than 40 inches as a male or larger than 35 inches as a female, you’re probably insulin resistant.  Most men complain they don’t have a tape measure to measure their belly, so I tell them if they walk toward the wall and the first thing that touches the wall is their belly, “you’re insulin resistant.”

Skin Tags
Skin Tags

Skin tags or the presence of thickened browning skin at areas of skin folds (acanthosis nigricans) are classic signs of insulin resistant.

Acanthosis Nigricans
Acanthosis Nigricans of the Neck-line

Hypoglycemia or low blood sugar is another sign of hyperinsulinemia or insulin resistance.  This is where a person gets light headed or dizzy 2-5 hours after eating a meal that contains mainly starch or sugar.

Insulin resistance requires a dramatically different dietary approach than the standard diets we’ve been taught all our lives. The “heart healthy” diet, DASH diet, vegetarian/vegan diet, low fat diet or calorie restricted diet just don’t work with hyperinsulinemia or insulin resistance.  If you are insulin resistant, a low fat/calorie restricted diet will not be very effective, and you may even gain weight with this approach as many of my patients have experienced.

If you have any of these symptoms, you need to follow up with your doctor or weight management specialist.  Find out where your insulin levels are in relationship to your diet.  Losing weight is possible.  You can get started here with my ketogenic dietary program.

As this is a journey, it will probably have a number of twists and turns that are often made easier with a road map.  Getting checked out with your doctor, and evaluating your metabolic status is your road map.  Check out the health programs I offer to my patients to get this road map. I’ve also produced hundreds of videos on YouTube and DocMuscles.Locals.com to help you down the road.   Either way, enjoy the journey!!

Inflammation Killer – A Ketogenic Diet

Image
Symptoms of Inflammation seen in Diabetes Mellitus

A recent study published in the Annals of Internal Medicine demonstrate significant improvement in overall inflammation in type II diabetic patients following a carbohydrate restricted diet versus a low fat calorie restricted diet.  Another bit of proof demonstrating what I’ve been seeing in my office over the last 8 years.  The study reveals significant improvement in glycemic (blood sugar) control in those following a low carbohydrate diet as well as significant lowering of C-reactive protein, IL-1 and IL-6 over those following a low fat diet. You can see the study here.