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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 the Himalayan Pink Salt because it contains 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 KetoKart 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.  This 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 Periscope video below:

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.