Tag: Low Carb Diet

March 28, 2016

Healthy Ketogenic Bio-Hacking…Come Learn How

Ever wondered if it is possible to change up your metabolic genetics for the better? Come join me this week. I’ll be speaking about Ketogenic BioHacking, Thursday, March 31st, in Scottsdale, Arizona. Meet me from 7-8:30pm and learn how to improve fat burning, bio-hack your epi-genetic metabolism for improved blood sugar, cholesterol, blood pressure and so much more . . .

You’ll also get to meet Kim Minert who will be signing her new book, Burn Fat for Fuel. And, you’ll get a chance to meet the amazing Abigail Epps-Kluttz, body builder, fitness model & Pruvit Ambassador.

You can sign up at the Eventbrite link here. I look forward to seeing you!!

February 20, 2016

Random Thoughts from the Toilet Paper Roll

I am a family physician. Each door I open holds another challenge, another question or another puzzle. You never know what will be behind door number 2 or number 3. This leads to becoming very adept at understanding and thinking about the random. Door #1 one holds the rash. Door #2 holds the patient with diabetes. Door #3 . . . rectal bleeding. Yes, my morning often starts out just that way.

While randomly thinking about the randomness that my career choice brought to my life, I’ve made a few random decisions that relate to our health in general.

First, if I ever decide to buy a toilet paper roll company, I’ve already made the executive decision that each piece of paper on the roll needs the opportunity to express itself in a random way. One piece would say, “Nice fingernail polish.” Another would say, “Wow, you have a nice bottom.” A third would say, “Please don’t apologize, brown is my favorite color.” A fourth might say, “You know, you really should see your doctor about that . . . ”

Second, if I live until I’m 70 years old, I will have spent 10 of those years on Monday. This calls for sausage and eggs for breakfast every Monday morning. Wait, I’m already doing that . . . no wonder I like Mondays. It also means that if I set my clock to wake up earlier on the weekend, then Monday morning I will start the week off “sleeping in.” It is amazing to me that even under ideal conditions people have trouble locating their car keys in a pocket, finding their cell phone, and even pinning the tail on the donkey . . . but I’d bet everyone of us can find & push the SNOOZE button from 3 feet away, in about 1.7 seconds, eyes closed, first time, every time…

Third, with all of this randomness . . . someone needs to invent the “Sarcasm Font.” There are some things that shouldn’t be written in “Times New Roman.”

Fourth, Can I take back all those times I didn’t want to take a nap when I was younger? I am quite convinced that a significant number of my obesity patient’s would be so much more successful with an afternoon nap.

Fifth, in the age of computers, voice recognition, iPhones and electronic medical records, I really want to meet the person that invented cursive and ask, “Was that really necessary?”

Sixth, in this new era of reality everything, I think that print newspapers would still be fascinatingly successful if the obituary column told you how the person died.

KetoOS – Drinkable Exogenous Ketones

Seventh, with all the high fat, moderate protein I recommend, the freezer has become an important appliance in the ketogenic world . . .yet no one can answer me this question: “Why is there still no freezer light?”

Last, bad decisions often make for the best stories. . . .

January 31, 2016

Ketogenic Lifestyle Rule #2: Life Begins at the Edge of Your Comfort Zone

We have been taught for over 50 years that the minimum carbohydrate intake necessary to maintain health is 130 grams per day, with the average diet of 2000 calories per day containing around 300 grams per day based on 1977 recommendations that 55-60% of are dietary intake should come from carbohydrates. This value was initially established during World War II by a committee of scientists tasked with determining dietary changes that might effect national defense (1). These “guidelines,” originally called the Recommended Daily Allowances (RDA) and accepted by many as the gospel truth, have been modified every ten years and in 1997 changed to the Dietary Reference Intake (DRI). However, the recommended carbohydrate values have not changed other than “avoiding added sugars” in the most recent 2015 recommendations.

In light of the fact that there are NO actual diseases caused by lack of carbohydrate intake, most dietitians and physicians still preach the carbohydrate dogma originally outlined by the RDA. I say dogma, because these recommendations are based on a diet that vilifies fat, particularly animal fat like red meat. Say the words “red meat” around a dietician these days you’d think Voldemort (“He Who Shall Not Be Named”) had returned.

I bring up the carbohydrate quandary because it is a question that I am asked every single day. The question that seems to be asked of me, more and more, is what exactly is a carbohydrate?

Let’s make it simple. There are really only three types of carbohydrates:

Sugar
Starch (known as complex carbohydrates)
Fiber

Let’s start with Sugar. The simple form of carbohydrates, and the form that spikes your blood sugar and insulin rapidly, are called mono-saccharides (glucose, galactose, fructose & xylose). When two of these mono-saccharides are bound together they form disaccharides like sucrose, also known as “table sugar” (glucose + fructose), lactose found in milk (glucose + galactose), and maltose found in cereals and sweet potatoes (glucose + glucose).

Milk Sugar or Lactose (glucose + glucose)

The simple monosaccharides or disaccharides are easy broken into their mono-saccharide form in the blood stream and require the body to produce insulin to be used. The person with insulin resistance, impaired fasting glucose or type II diabetes often produces 2-10 times the normal amount of insulin to correctly use these mono-saccharides (see why this is a problem in: The Dreaded Seven: Seven Detrimental Things Caused By High Insulin Levels). Remember, fruit is also simple sugar containing the mono-saccharide fructose . . . which we call “natures candy” in my office.

“Yea, I know sugar is bad for me, but Dr. Nally, I just eat the good starches.”

If I had a nickel for every time I’ve herd that phrase . . .

We’ve become comfortable with shunning fat and “simple sugar,” but in the process we’ve been eating more “good starch.” But the “good starches” are also saccharides – just in longer chains of more than three glucose molecules bound together. Our gut easily breaks the bonds between the glucose links and turns these starches into mono-saccharides to be used as fuel. It takes a bit longer than the simple sugars above, so the release of insulin is slower (which is why it has a better glycemic index score), but whether you produce the insulin in the first hour or the second hour after eating it, insulin is still insulin. In the case of insulin resistance, the damage is still done.

These good starches make up “comfort food” like bread, rice, pasta, potatoes, corn, grains & oats. To the patient with insulin resistance, impaired fasting glucose or type II diabetes, the higher insulin response stimulates increased weight gain, rise in cholesterol, shift in hormone function and progression of atherosclerosis (vascular and heart disease). See the recent article on Why Your Oatmeal is Killing Your Libedo.

What about “resistance starches?” These are still starches and I am finding clinically that they still cause a rise in insulin and push people out of ketosis (See Common Ketosis Killers).

Finally, Fiber. Fiber is a carbohydrate, however, it is the indigestible part of the plant. Fiber has double bonds between the saccharides that human gastrointestinal tracts cannot digest. In most cases, fiber passes right through the intestines without being digested. It actually acts like a broom for your colon, helping the intestines to move nutrients through the system. This is why I recommend 1-2 leafy green salads a day for most patient’s following ketogenic diet. Fiber does help to promote bowel function.

The Leafy Greens

Fruit, non-green vegetables, pasta, grains and breads do contain good sources of fiber, however, these foods also have absorbable starches making them problematic as noted above.

The take home message is this, the use of starch or simple carbohydrate will be problematic for weight loss, cholesterol control, blood sugar control or blood pressure control in a patient with insulin resistance.

Therefore, the ketogenic lifestyle truly begins at the end of your comfort zone.

January 30, 2016

Ketogenic Lifestyle Rule #1: There should ALWAYS be bacon in the fridge

I thought that over the next few weeks I’d address a number of Ketogenic Lifestyle Rules that I have adopted. These seem to help and bring a little clarity to one following a Ketogenic Lifestyle or someone on the road to becoming a true “Ketonian.”

The first of these rules is that there should ALWAYS be bacon in the fridge!

We address this rule and some interesting facts around having bacon in the fridge in this evening’s Persicope below. We also address the benefits of journaling, how to help stop binge eating, what are your real protein needs, and red-meat fear-mongering. We even discuss whether or not pigs like bacon. Enjoy!

Links referenced in this video:

Red & Processed Meats: Bacon Fear-Mongering

Calculating Your Protein Needs from Ideal Body Weight

The Power of a Good Vitamin

(Just a note: I love Katch.me’s service; however, due to the contract language allowing Katch.me to have unlimited rights to my Periscope Videos, I have withdrawn from Katch and my videos are no longer available on this medium until the contract usage can be modified.)

January 8, 2016

Ketogenic Diet Halts Tumor Growth

Prostate Cancer Cell Replication

It has long been understood that tumor cells of any kind require high levels of glucose to grow and spread (1,2). It is also recognized that higher levels of insulin, commonly found in patients with insulin resistance or type II diabetes, are 2.4 times more likely to stimulate the development of breast cancer (3). A diet low in glucose has thereby been theorized to be an adjunct to cancer treatment.

Ketogenic diets have been demonstrated to be therapeutically useful in the treatments of epilepsy and cardiovascular disease (4). A ketogenic diet is one in which carbohydrate levels are kept below 50 grams per day and fat intake is increased to the point that the body shifts its metabolism to use triglycerides, and the ketones derived from triglycerides, as the primary fuel source for the majority of the cells within the body. With this understanding in mind, the application of a ketogenic diet, one high in fat and protein with limited carbohydrate or glucose has been suggested as a adjunct to cancer treatments (5).

KetoOS – Drinkable Exogenous Ketones

A recent study (6) in the Oncology Letters evaluated the benefits of a ketogenic diet in 78 cancer patients in clinical practice. A novel marker measuring the tumor cells use of glucose called transketolase-like-1 (TKTL1) was closely monitored, as was each of the 78 patients adherence to a ketogenic diet. Increased TKTL1 was noted in more aggressively active and growing tumors (7,8).

Among the 43 males and 35 females, 7 patients agree to and followed a fully ketogenic diet and 6 of them followed a partially ketogenic diet. Ketogenic meals were provided by a German company called Tavarlin that would prepare and mail ketogenic meals including oil, fat, snacks, bread, protein and energy drinks. Dietary journals were reviewed every three months over a period of about 10 months.

40 % of these patients experienced a halting of the tumor progression and 60% experienced improvement noted by normalization of TKTL1 or reduction in TKTL1, respectively. Those on a ketogenic diet demonstrated an average reduction of TKTL1 by approximately 50%.

This is the first study of its kind and has significant potential. Could dietary carbohydrate restriction be an effective cancer treatment or adjunct to cancer treatment?

Because the food diaries were based on reporting only, the sample study was very small, and patients treated in the outpatient setting have the possibility of variability in the standard oncologic treatments, the results must be interpreted with caution. However, the data is very promising. This study is one in which I have great interest as I have seen similar results in my clinic on a case by case basis.

Based on the limitations noted above, rigorous randomized control studies are needed, but this is an exciting an promising first step. Additionally, the presence of a marker for tumor growth that correlates with diet is remarkable. And, it provides the ketogenic specialist a possible measurement tool that could be used clinically.

References:

Klement RJ and Kämmerer U: Is there a role for carbohydrate restriction in the treatment and prevention of cancer? Nutr Metab (Lond) 8: 75, 2011
Vaughn AE and Deshmukh M: Glucose metabolism inhibits apoptosis in neurons and cancer cells by redox inactivation of cytochrome c. Nat Cell Biol 10: 1477-1483, 2008.
Gunter MJ, Hoover DR, Yu H, Wassertheil-Smoller S, Rohan TE, Manson JE, Li J, Ho GY, Xue X, Anderson GL, et al: Insulin, insulin-like growth factor-I, and risk of breast cancer in postmenopausal women. J Natl Cancer Inst 101: 48-60, 2009.
Paoli A, Rubini A, Volek JS and GrimaldiKA: Beyond weight loss: A review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets. Eur J Clin Nutr 67: 789-796, 2013.
Ruskin DN and Masino SA: The nervous system and metabolic dysregulation: Emerging evidence converges on ketogenic diet therapy. Front Neurosci 6: 33, 2012.
Jansen, N., Walach, H.”The development of tumours under a ketogenic diet in association with the novel tumour marker TKTL1: A case series in general practice”. Oncology Letters 11.1 (2016): 584-592.
. Schwaab J, Horisberger K, Ströbel P, Bohn B, Gencer D, Kähler G, Kienle P, Post S, Wenz F, Hofmann WK, et al: Expression of Transketolase like gene 1 (TKTL1) predicts disease-free survival in patients with locally advanced rectal cancer receiving neoadjuvant chemoradiotherapy. BMC Cancer 11: 363, 2011.
Zhang S, Yang JH, Guo CK and Cai PC: Gene silencing of TKTL1 by RNAi inhibits cell proliferation in human hepatoma cells. Cancer Lett 253: 108-114, 2007

January 6, 2016

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.

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).

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.

References:

J. M. Pearce, “Historical descriptions of multiple sclerosis,” European Neurology, vol. 1, no. 1, pp. 49–53, 2005.
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.
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.
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.
C. Confavreux and S. Vukusic, “Natural history of multiple sclerosis: a unifying concept,” Brain, vol. 129, no. 3, pp. 606–616, 2006.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.
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.

January 5, 2016

What Are Your Biggest Weight Loss Struggles?

Join Dr. Nally on this evening’s Periscope as we talk about your biggest weight loss struggles in rapid fire style. We cover topics this evening from the effects of cheating on a ketogenic diet to how to overcome a weight loss stall . . . join us to hear the whole conversation.

December 15, 2015

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:

December 13, 2015

Caffeine . . . Weight Loss Wonder Boy or Sneaky Scoundrel?

I’ve been looking for the answer for quite some time. . . what role does caffeine play in your and my weight management journey? The answer gave me a headache. . . literally and figuratively.

As many of you, including my office staff, know, I love my Diet Dr. Pepper (and my bacon). I found that being able to sip on a little soda throughout the day significantly helped the carbohydrate cravings and munchies during a busy and stressful day at the office. Diet Dr. Pepper contains caffeine, however, I wasn’t really worried. Caffeine has been well know to have a thermogenic effect which increases your metabolism and has been thought for many years to help with weight loss among the weight loss community.

Diet Dr. Pepper is, also, one of only four diet sodas on the grocery store shelves that doesn’t contain acesulfame potassium (click here to see why most artificial sweeteners cause weight gain). The four diet sodas that I have been comfortable with my patients using are Diet Dr. Pepper, Diet Coke, Diet Mug Root-beer and Diet A&W Cream Soda. These are the last four hold out diet sodas that still use NutraSweet (aspartame) as the sweetener. Most of the soda companies have switched the sweetener in their diet sodas to the insulinogenic acesulfame potassium because it tastes more natural and aspartame has been given a media black eye of late. However, NutraSweet (aspartame) is the only sweetener that doesn’t spike your insulin or raise blood sugar (click here to find out why that is important).

Yes, I know. The ingestion of 600 times the approved amount of aspartame causes blindness in lab rats (but we’re not lab rats, and . . . have you ever met someone that drinks 600 Diet Dr. Peppers in a day? The lethal dose of bananas, which are high in potassium that will stop your heart, is 400). Aspartame can also exacerbate headaches in some (about 5% of people) and I’ve had a few patients with amplified fibromyalgia symptoms when they use aspartame. But for most of us, its a useful sweetener that doesn’t spike your insulin response, halting or causing weight gain.

But, over the last few years, I’ve noticed that increased amounts of Diet Dr. Pepper & Diet Coke seem to cause plateauing of weight and decreasing the ability to shift into ketosis, especially mine. I’ve also noticed (in my personal n=1 experimentation) that my ability to fast after using caffeine regularly seems to be less tolerable, causing headaches and fatigue 8-10 hours into the fast, symptoms that don’t seem to let up until eating. Through the process of elimination, caffeine seems to be the culprit.

After mulling through the last 10 years of caffeine research, most of which were small studies, had mixed results, used coffee as the caffeine delivery system (coffee has over 50 trace minerals that has the potential to skew the results based on the brand) and never seemed to ask the right questions, the ink from a study in the August 2004 Diabetes Care Journal screamed for my attention.

It appears that caffeine actually stimulates a glucose and insulin response through a secondary mechanism. The insulin surge and glucose response is dramatically amplified in patients who are insulin resistant. Caffeine doesn’t effect glucose or insulin if taken while fasting; however, when taken with a meal, glucose responses are 21% higher than normal, and insulin responses are 48% higher in the insulin resistant patient. Caffeine seems to only effect the postprandial (2 hours after a meal) glucose and insulin levels. The literature shows mixed responses in patients when caffeine is in coffee or tea, probably due to the effect of other organic compounds (1).

Caffeine effect on plasma glucose and plasma insulin compared to placebo (1).

Caffeine also diminishes insulin sensitivity and impairs glucose tolerance in normal and already insulin resistant and/or obese patients. This is seen most prominently in patients with diabetes mellitus type II (stage IV insulin resistance). Caffeine causes alterations in glucose homeostasis by decreasing glucose uptake into skeletal muscle, thereby causing elevations in blood glucose concentration and causing an insulin release (2-6).

Studies show that caffeine causes a five fold increase in epinephrine and a smaller, but significant, norepinephrine release. The diminished insulin sensitivity and exaggerated insulin response appears to be mediated by a catacholamine (epinephrine, norepinephrine & dopamine) induced stress response (5). Caffeine has a half life of about 6 hours, that means the caffeine in your system could cause a catacholamine response for up to 72 hours depending upon the amount of caffeine you ingest (7).

The reason for my, and other patient’s, headaches and fatigue after a short fast was due to the exaggerated stress hormone response. Increased levels of insulin were induced by a catacholamine cascade after caffeine ingestion with a meal, dramatically more amplified in a person like me with insulin resistance. The caffeine with the last meal cause hypoglycemia 5-7 hours into the fasting, leading to headaches and fatigue that are only alleviated by eating.

Even when not fasting, the caffeine induced catacholamine cascade causes up to 48% more insulin release with a meal, halting weight loss and in some cases, causing weight gain.

Caffeine is not the “Wonder-Boy” we thought it was.

How much caffeine will cause these symptoms? 50 mg or more per day can have these effects.

Ingestion of caffeine has the following effects:

20-40 mg – increased mental clarity for 2-6 hours
50-100 mg – decreased mental clarity, confusion, catacholamine response
250-700 mg – anxiety, nervousness, hypertension & insomnia
500 mg – relaxation of internal anal sphincter tone (yes . . . you begin to soil yourself)
1000 mg – tachycardia, heart palpitations, insomnia, tinnitus, cognitive difficulty.
10,000 mg (10 grams) – lethal dose (Yes, 25 cups of Starbucks Coffee can kill you)

The equivalent of 100 mg of in a human was given to a spider, you can see the very interesting effect on productivity. How often does the productivity of the day feel like the image below?

Normal Spider (9)

Spider on caffeine (9)

Beware that caffeine is now being added to a number of skin care products including wrinkle creams and makeup. Yes, caffeine is absorbed through the skin, so check the ingredients on your skin care products.

Diet Dr. Pepper, my caffeine delivery system of choice, has slightly less caffeine (39 mg per 12 oz can or 3.25 mg per oz) than regular Dr. Pepper. I found myself drinking 2-3 liters of Diet Dr. Pepper per day (long 16-18 hour work days in the office). After doing my research, I realized that my caffeine tolerance had built up to quite a significant level (230-350 grams per day).

So, a few weeks ago, I quit . . . cold turkey.

Did I mention the 15 withdrawal symptoms of caffeine? (8)

Headache – behind the eyes to the back of the head
Sleepiness – can’t keep your eyes open kind of sleepiness
Irritability – everyone around you thinks you’ve become a bear
Lethargy – feels like your wearing a 70 lb lead vest
Constipation – do I really need to explain this one?
Depression – you may actually feel like giving up on life
Muscle Pain, Stiffness, Cramping – feel like you were run over by a train
Lack of Concentration – don’t plan on studying, doing your taxes or performing brain surgery during this period
Flu Like Illness – sinus pressure and stuffiness that just won’t clear
Insomnia – you feel sleepy, but you can’t sleep
Nausea & Vomiting – You may loose your appetite
Anxiety – amplified panic attacks or feeling like the sky is falling
Brain Fog – can’t hold coherent thoughts or difficulty with common tasks
Dizziness – your sense of equilibrium may be off
Low Blood Pressure & Heart Palpitations – low pressure and abnormal heart rhythm

I experienced 13 of the 15 that lasted for 4 days. I do not recommend quitting cold turkey unless you have a week off and someone to hold your hand, cook your meals and dose your Tylenol or Motrin. My wife thought I was dying. . . I thought I was dying on day two. I actually had a nightmare about buying and getting into my own coffin. It can take up to three weeks to completely recover from caffeine withdrawal.

The other way to quit is to decrease your caffeine intake by 50 mg every two days. That means decrease caffeine by:

1 can of soda every two days
1/4 cup of coffee every day
1/2 can of Energy Drinks every two days
1 cup of tea every two days

The benefit of this method is that withdrawal symptoms are much less severe without the caffeine headache and the ability to remain productive. It will take longer, but quitting cold turkey is not a pretty picture. Been there . . . done that, . . . and I’m not going back. I actually lost another half inch off my waistline by day 5 of caffeine discontinuation.

What is the take home message here? If you have any degree of insulin resistance, caffeine makes it worse and will amplify your weight gain as well as decrease the productivity of your day.

References:

December 11, 2015

Listen & Vote for Jenna!!!

Our intelligent and beautiful physician assistant, Jenna Lightfoot, PA-C, is in the running for a co-host position with Jimmy Moore on LowCarbConversations.com you can hear her on today’s podcast with Jimmy Moore and cast your vote here: Round 2 Co-host Contest.

You can also download the podcast on iTunes here.

December 2, 2015

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 . . .

November 25, 2015

Adrenal Insufficiency, Adrenal Fatigue, PseudoCushing’s Syndrome – Oh My!

Adrenal Fatigue? Adrenal Insufficiency? Cortisol? PseudoCushing’s Syndrome? What do these terms mean and why are they all over the internet these days? And, what do they have to do with your weight loss?

This was our topic this evening on PeriScope. Katch Dr. Nally speak about this topic with rolling comments at Katch.me/docmuscles. Or you can watch the video below:

If you’re not sure about what this is, you’re not alone. I think I’ve heard the term “Adrenal Fatigue” at lease four times a day for the last three months. If you ask your doctor, they’ll probably scratch their heads too. The funny thing is that “Adrenal Fatigue” isn’t a real diagnosis, but it is all over the internet and it shows up in the titles of magazines in the grocery store every day. There’s even and “Adrenal Fatigue For Dummies” so it must be real, right?!

No. It isn’t a real diagnosis. It is a conglomeration of symptoms including fatigue, difficulty getting out of bed in the morning, and “brain fog” that have been lumped together to sell an “adrenal supplement.” (Sorry, but that’s really what it is all about.) Do a Google search and the first five or six sites describing adrenal fatigue claim the solution is taking their “special adrenal supplement.”

I know what you’re thinking, “Your just a main stream, Western Medicine doctor, Dr. Nally, you wouldn’t understand.” Actually, I do understand.

Adrenal fatigue has risen in popularity as a “lay diagnosis” because many patients show up at their doctors office with significant symptoms that actually interfere with their ability to function, and after all the testing comes back negative for any significant illness, they are told that they are normal. But the patient still has the symptoms and no answer or treatment has been offered. It’s discouraging. . . very discouraging.

That’s because the symptoms are actually the body’s response to chronic long term stress. Many of my patients, myself included, have found themselves “stuck” in their weight loss progression, feeling fatigued, struggling to face the day, with a number of symptoms including cold intolerance, memory decline, difficulty concentrating, depression, anxiety, dry skin, hair loss, and even infertility in some cases. Is it poor functioning adrenal glands? No, your feeling this way because the adrenal glands are actually doing their job!!

If the adrenal glands weren’t working you’d experience darkening of the skin, weight loss, gastric distress, significant weakness, anorexia, low blood pressure, and low blood sugar. The symptoms are actually called Addison’s disease and it is actually fairly rare (1 in 100,000 chance to be exact). So what is causing the symptoms you ask?

There are a number of reasons, but one that I am seeing more and more frequently is “Pseudo-Cushings’s Syndrome.” Pseudo-Cushing’s Syndrome is a physiologic hypercortisolism (over production of cortisol) that can be caused by five common issues:

Chronic Physical Stress
Severe Bacterial or Fungal Infections that Go Untreated
Malnutrition or Intense Chronic Exercise
Psychological Stress – including untreated or under-treated depression, anxiety, post-traumatic stress, or dysthymia (chronic melancholy)
Alcoholism

The psychiatric literature suggest that up to 80% of people with depressive disorders have increased cortisol secretion (1,2,3). People with significant stressors in their life have been show to have an increased corsiol secretion. Chronic stress induces hyperactivity of the hypothalamic-pituitary-adrenal axis causing a daily, cyclic over production of cortisol and then normalization of cortisol after resolution of the stressor. This cortisol response is not high enough to lead to a true Cushing’s Syndrome, but has the effect of the symptoms listed above and begins with limiting ones ability to loose weight.

I’m convinced that this is becoming more and more prevalent due to the high paced, high-stress, always on, plugged in, 24 hour information overload lives we live.

What is cortisol? It is a steroid hormone made naturally in the body by the adrenal cortex (outer portion of the adrenal gland). Cortisol is normally stimulated by a number of daily activities including fasting, awakening from sleep, exercise, and normal stresses upon the body. Cortisol release into the blood stream is highest in the morning, helping to wake us up, and tapers into the afternoon. Cortisol plays a very important role in helping our bodies to regulate the correct type (carbohydrate, fat, or protein) and amount of fuel to meet the bodies physiologic demands that are placed upon it at a given time (4,5,6).

Under a stress response, cortisol turns on gluconeogensis in the liver (the conversion of amino acids or proteins into glucose) for fuel. Cortisol, also, shifts the storage of fats into the deeper abdominal tissues (by stimulating insulin production) and turns on the maturation process of adipocytes (it makes your fat cells age – nothing like having old fat cells, right?!) In the process, cortisol suppresses the immune system through an inhibitory effect designed to decrease inflammation during times of stress (7,8,9). If this was only occurring once in a while, this cascade of hormones acts as an important process. However, when cortisol production is chronically turned up, it leads to abnormal deposition of fat (weight gain), increased risk of infection, impotence, abnormal blood sugars, brain fog, head
aches, hypertension, depression, anxiety, hair loss, dry skin and ankle edema, to name a few.

The chronic elevation in cortisol directly stimulates increased insulin formation by increasing the production of glucose in the body, and cortisol actually blunts or block-aids the thyroid function axis. Both of these actions halt the ability to loose weight, and drive weight gain.
Cortisol also increases appetite (10). That’s why many people get significant food cravings when they are under stress (“stress eaters”). Cortisol also indirectly affects the other neuro-hormones of the brain including CRH (corticotrophin releasing hormone), leptin, and neuropeptide Y (NPY). High levels of NPY and CRH and reduced levels of leptin have also been shown to stimulate appetite and cause weight gain (10-11).

How do you test for Pseudo-Cushing’s Syndrome?

Testing can be done by your doctor with a simple morning blood test for cortisol. If your cortisol is found to be elevated, it needs to be repeated with an additional 24 hour urine cortisol measurement to confirm the diagnosis. If Cushing’s Syndrome is suspected, some additional blood testing and diagnostic imaging will be necessary. Pseudo-Cushing syndrome will demonstrate a slightly elevated morning cortisol that doesn’t meet the criteria for true Cushing’s type syndrome or disease.

How do you treat it?

First, the stressor must be identified and removed. Are you getting enough sleep? Is there an underlying infection? Is there untreated anxiety or depression present? Are you over-exercising? These things must be addressed.

Second, underlying depression or anxiety can be treated with counseling, a variety of weight neutral anti-depressant medications or a combination of both. Many of my patients find that meditation, prayer, and journaling are tremendous helps to overcoming much of the anxiety and depression they experience.

Third, adequate sleep is essential. Remove the television, computer, cell phone, iPad or other electronic distraction from the bedroom. Go to bed at the same time and get up at the same time each day. Give yourself time each day away from being plugged in, logged in or on-line.

Fourth, mild intensity (40% of your maximal exertion level) exercise 2-3 days a week was found to lower cortisol; however, moderate intensity (60% of your maximal exertion level) to high intensity (80% of your maximal exertion level) exercise was found to raise it (12). A simple 20 minute walk, 2-3 times per week is very effective. Find a hobby that you enjoy and participate in it once or twice a week. Preferably, a hobby that requires some physical activity. The activity will actually help the sleep wake cycles to improve.

Fifth, follow a low carbohydrate or ketogenic diet. Ketogenic diets decrease insulin and reverse the effect of long term cortisol production. Ketogenic diets a have also been shown to decrease or mitigate inflammation by reducing hyperinsulinemia commonly present in these patients (13).

So, the take home message is . . . take your adrenal glands off of overdrive.

References:

Pfohl B, Sherman B, Schlechte J, Winokur G. Differences in plasma ACTH and cortisol between depressed patients and normal controls. Biol Psychiatry 1985; 20:1055.
Pfohl B, Sherman B, Schlechte J, Stone R. Pituitary-adrenal axis rhythm disturbances in psychiatric depression. Arch Gen Psychiatry 1985; 42:897.
Gold PW, Loriaux DL, Roy A, et al. Responses to corticotropin-releasing hormone in the hypercortisolism of depression and Cushing’s disease. Pathophysiologic and diagnostic implications. N Engl J Med 1986; 314:1329.
Ely, D.L. Organization of cardiovascular and neurohumoral responses to stress: implications for health and disease. Annals of the New York Academy of Sciences (Reprinted from Stress) 771:594-608, 1995.
McEwen, B.S. The brain as a target of endocrine hormones. In Neuroendocrinology. Krieger and Hughs, Eds.: 33-42. Sinauer Association, Inc., Massachusetts, 1980.
Vicennati, V., L. Ceroni, L. Gagliardi, et al. Response of the hypothalamic- pituitary-adrenocortical axis to high-protein/fat and high carbohydrate meals in women with different obesity phenotypes. The Journal of Clinical Endocrinology and Metabolism 87(8) 3984-3988, 2002.
Wallerius, S., R. Rosmond, T. Ljung, et al. Rise in morning saliva cortisol is associated with abdominal obesity in men: a preliminary report. Journal of Endocrinology Investigation 26: 616-619, 2003.
Epel, E.S., B. McEwen, T. Seeman, et al. Stress and body shape: stress-induced cortisol secretion is consistently greater among women with central fat.
Psychosomatic Medicine 62:623-632, 2000.
Tomlinson, J.W. & P.M. Stewart. The functional consequences of 11_- hydroxysteroid dehydrogenase expression in adipose tissue. Hormone and Metabolism Research 34: 746-751, 2002.
Epel, E., R. Lapidus, B. McEwen, et al. Stress may add bite to appetite in women: a laboratory study of stress-induced cortisol and eating behavior.Psychoneuroendocrinology 26: 37-49, 2001.
Cavagnini, F., M. Croci, P. Putignano, et al. Glucocorticoids and neuroendocrine function. International Journal of Obesity 24: S77-S79, 2000.
Hill EE, Zack E, Battaglini C, Viru M, Vuru A, Hackney AC. Exercise and circulating cortisol levels: the intensity threshold effect. J Endocrinol Invest. 2008. Jul;31(7):587-91.
Fishel MA et al., Hyperinsulinemia Provokes Synchronous Increases in Central Inflammation and β-Amyloid in Normal Adults. Arch Neurol. 2005;62(10):1539-1544. doi:10.1001/archneur.62.10.noc50112.

November 24, 2015

The 5 Myths of Weight Loss

This evening we covered the 5 myths of weight loss identified through the National Weight Control Registry’s research findings. What causes “wrinkle face” for Dr. Nally? We also talked about & answered 20 minutes of rapid fire questions ranging from the amount of protein you need daily to the likelihood a human could be a bomb calorimeter . . . exciting stuff!!

You can watch the video stream below. Or you can Katch the replay with the rapid stream of exciting comments here at Katch.me/docmuscles.

November 23, 2015

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 . . .

November 23, 2015

Diabetes Mellitus – Really the Fourth Stage of Insulin Resistance

I just completed my reading of Dr. Joseph Kraft’s Diabetes Epidemic & You. This text originally printed in 2008 and was re-published in 2011. I am not really sure why I have never seen this book until now, but I could not put it down. I know, I am a real life medical geek. But seriously, you should only read this book if you are concerned about your health in the future. Otherwise, don’t read it.

For the first time in 15 years, someone has published and validated what I have been seeing clinically in my office throughout my career. Dr. Kraft is a pathologist that began measuring both glucose and insulin levels through a three hour glucose tolerance blood test at the University of Illinois, St. Joseph Hospital in Chicago. This test consists of checking blood sugar and insulin in a fasted state, and then drinking a 100 gram glucose load followed by checking blood sugar and insulin at the 30, 60, 120 and 180 minute marks (a total of three hours).

Dr. Kraft completed and recorded this test over a period of almost 30 years on 14,384 patients between 1972 and 1998. His findings are landmark and both confirm and clarify the results that I have seen and suspected for years.

I am convinced that our problem with treating obesity, diabetes and the diseases of civilization has been that we defined diabetes as a “disease” based on a lab value and a threshold instead of identifying the underlying disease process. We have been treating the symptoms of the late stage of a disease that started 15 to 20 years before it is ever actually diagnosed. Diabetes is defined as two fasting BS >126, any random blood sugar >200, or a HbA1c >6.5%. (Interestingly this “disease” has been a moving target. When I graduated from medical school it was two fasting blood sugars >140 and the test called hemoglobin A1c (HbA1c) that we use today for diagnosis didn’t even exist). The semantics associated with this problem is that many of us recognize that the disease is not actually diabetes. The disease is (as far as we understand it today) insulin resistance or hyperinsulinemia. This is where Dr. Kraft’s data is so useful. Diabetes, as it is defined above, is really the fourth stage of insulin resistance progression over a 15-20 year period and Dr. Kraft’s data presents enormous and very clear evidence to that effect.

When I first entered private practice 15 years ago, I noticed a correlation and a very scary trend that patients would present with symptoms including elevated triglycerides, elevated fasting blood sugar, neuropathy, microalbuminuria, gout, kidney stones, polycystic ovarian disease, coronary artery disease and hypertension that were frequently associated with diabetes 5-15 years before I ever made the diagnosis of diabetes mellitus. I began doing 2 hour glucose tolerance tests with insulin levels and was shocked to find that 80-85% of those people were actually diabetic or very near diabetic in their numbers. The problem with a 2 hour glucose tolerance test, is that if you are diabetic or pre-diabetic, you feel miserable due to the very profound insulin spike that occurs. A few patients actually got quite upset with me for ordering the test, both because of how they felt after the test, and the fact that I was the only physician in town ordering it. So, in an attempt to find an easier way, I found that the use of fasting insulin > 5 nU/dl, triglycerides > 100 mg/dl and small dense LDL particle number > 500 correlated quite closely clinically with those patients that had positive glucose tolerance tests in my office. There is absolutely no data in the literature about the use of this triangulation, but I found it to be consistent clinically.

I was ecstatic to see that Dr. Kraft plowed through 30 years and over 14,000 patients with an unpleasant glucose tolerance test and provided the data that many of us have had to clinically triangulate. (I’m a conservative straight white male, but if Dr. Kraft would have been sitting next to me when I finished the book this afternoon, I was so excited that I probably would have kissed him.)

Insulin resistance or hyperinsulinemia (the over production of insulin between 2-10 times the normal amount after eating carbohydrates) is defined as a “syndrome” not a disease. What Dr. Kraft points out so clearly is that huge spikes in insulin occur at 1-2 hours after ingestion of carbohydrates 15-20 years prior to blood sugar levels falling into the “diabetic range.” He also demonstrates, consistently, the pattern that occurs in the normal non-insulin resistant patient and in each stage of insulin resistance progression.

The information extrapolated from Dr. Kraft’s research give the following stages:

Stages of insulin resistance by 3 hr OGTT extrapolated from “Diabetes Epidemic & You”

From the table above, you can see that the current definition of diabetes is actually the fourth and most prolifically damaging stage of diabetes. From the data gathered in Dr. Kraft’s population, it is apparent that hyperinsulinemia (insulin resistance) is really the underlying disease and that diabetes mellitus type II should be based upon an insulin assay instead of an arbitrary blood sugar number. This would allow us to catch and treat diabetes 10-15 years prior to it’s becoming a problem. In looking at the percentages of these 14,384 patient, Dr. Kraft’s data also implies that 50-85% of people in the US are hyperinsuliemic, or have diabetes mellitus “in-situ” (1). This means that up to 85% of the population in the U.S. is in the early stages of diabetes and is the reason 2050 projections state that 1 in 3 Americans will be diabetic by 2050 (2).

Insulin resistance is a genetically inherited syndrome, and as demonstrated by the data above has a pattern to its progression. It is my professional opinion that this “syndrome” was, and actually is, the protective genetic mechanism that protected groups of people and kept them alive during famine or harsh winter when no other method of food preservation was available. It is most likely what kept the Pima Indians of Arizona, and other similar groups, alive while living for hundreds of years in the arid desert. This syndrome didn’t become an issue among these populations until we introduced them to Bisquick and Beer.

The very fascinating and notably exciting aspect of this whole issue is that insulin resistance is made worse by diet and it is completely treatable with diet. This is where the low carbohydrate diet, and even more effective ketogenic diet or lifestyle becomes the powerful tool available. Simple carbohydrate restriction reverses the insulin spiking and response. In fact, I witness clinical improvement in the insulin resistance in patients in my office over 18-24 months every day. You can get a copy of my Ketogenic Diet here in addition to video based low carbohydrate dietary instruction.

Until we are all on the same page and acknowledge that diabetes is really the fourth stage of progression on the insulin resistance slippery slope, confusion and arguments about treatment approaches will continue to be ineffective in reducing the diseases of civilization.

References:

November 22, 2015

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.”

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:

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.
Nasr SH, D’Agati VD. “Nodular glomerulosclerosis in the nondiabetic smoker.” J Am Soc Nephrol. 2007;18(7):2032.
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

November 20, 2015

How to Stay Motivated on Carbohydrate Restriction

This evening on PeriScope, we talked about the 10 things you can do to stay motivated on your low-carb lifestyle. A number of great questions were asked including:

How much carbohydrate should be restricted?
What labs should you be monitoring regularly?
What’s a normal blood sugar?
Why is Dr. Nally freezing in Denver?
Is fermented food good for you?
Why should you eat pickles and kimchi even when you’re not pregnant?

And, much much more . . . It’s like a college ketogenic course on overdrive . . . for FREE!!!

You can see the PeriScope with the comments rolling in real-time here: katch.me/docmuscles

Or, you can watch the video stream below:

See you next time.

November 18, 2015

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!!!

November 15, 2015

Four Most Common Weight Loss Mistakes that Halt Your Weight Loss

What are the four most common mistakes I see in the office when it comes to weight loss? Watch Dr. Nally on today’s PeriScope as he answers that question and many others. You can see it here with the live stream comments on: https://www.katch.me/docmuscles/v/392e5d3e-bb28-3176-a03a-83433878a5ce

Or see the video below:

November 9, 2015

How Fat Makes You Skinny . . . (Eating Fat Lowers Your Cholesterol?!)

Diseases seem to arrive in three’s each day in my office. Today I had three different patients with cholesterol concerns who were notably confused about what actually makes the cholesterol worse, and what causes weight gain. Each of them, like many patients that I see, were stuck in a state of confusion between low fat and low carbohydrate lifestyle change. My hope is to give my patients and anyone reading this blog a little more clarity regarding what cholesterol is, how it is influenced and how it affect our individual health.

First, the standard cholesterol profile does not give us a true picture of what is occurring at a cellular level. The standard cholesterol panel includes: total cholesterol (all the forms of cholesterol), HDL (the good stuff), LDL-C (the “bad” stuff) and triglycerides. It is important to recognize that the “-C” in these measurements stands for “a calculation” usually completed by the lab, and not an actual measurement. Total cholesterol, HDL-C and triglycerides are usually measured and LDL-C is calculated using the Friedewald equation [LDL = total cholesterol – HDL – (triglycerides/5)]. (No, there won’t be a quiz on this at the end . . . so relax.)

However, an ever increasing body evidence reveals that the concentration and size of the LDL particles correlates much more powerfully to the degree of atherosclerosis progression (arterial blockage) than the calculated LDL concentration or weight (1, 2, 3).

There are three sub-types of LDL that we each need to be aware of: Large “fluffy” LDL particles (type I), medium LDL particles (type II & III), and small dense LDL particles (type IV).

Weight & Size of VLDL, LDL & HDL

Why LDL-C is misleading: Identical LDL-C of 130 mg/dL can have a low risk (Pattern A) with a few “big fluffy LDL particles or high risk (Pattern B) with many small dense LDL particles.

Second, it is important to realize that HDL and LDL types are actually transport molecules for triglyceride – they are essentially buses for the triglycerides (the passengers). HDL can be simplistically thought of as taking triglycerides to the fat cells and LDL can be thought of as taking triglycerides from the fat cells to the muscles and other organs for use as fuel.

Third, it is the small dense LDL particles that are more easily oxidized and because of their size, are more likely to cause damage to the lining of the blood vessel leading to damage and blockage. The large boyant LDL (“big fluffy LDL particles”) contain more Vitamin E and are much less susceptible to oxidation and vascular wall damage.

Eating more fat or cholesterol DOES NOT raise small dense LDL particle number. Eating eggs, bacon and cheese does not raise your cholesterol! What increases small dense LDL particles then? It is the presence of higher levels of insulin. Insulin is increased because of carbohydrate (sugars, starches or fruits) ingestion. It is the bread or the oatmeal you eat with the bacon that is the culprit. The bread or starch stimulates and insulin response. Insulin stimulates the production of triglycerides and “calls out more small buses” to transport the increased triglyceride to the fat cells (4, 5, 6, 7).

Fourth, following a very low carbohydrate diet or ketogenic diet has been demonstrated to decreased small dense LDL particle number and correlates with a regression in vascular blockage (8, 9). So, what does this really mean to you and me? It means that the low-fat diet dogma that that has been touted from the rooftops and plastered across the cover of every magazine and health journal for the last 50 years is wrong. . . absolutely wrong.

I talk about this and answers questions on today’s Periscope. You can see the recording on Katch.me with the comments in real time here:

https://www.katch.me/docmuscles/v/2f0b6d07-d56a-368b-b4f6-34a5ab3da916

Or, you can watch the video below:

References:

Superko HR, Gadesam RR. Is it LDL particle size or number that correlates with risk for cardiovascular disease? Curr Atheroscler Rep. 2008 Oct;10(5):377-85. PMID: 18706278
Rizzo M, Berneis K. Low-density lipoprotein size and cardiovascular risk assessment. QJM. 2006 Jan;99(1):1-14. PMID: 16371404
Rizzo M, Berneis K, Corrado E, Novo S. The significance of low-density-lipoproteins size in vascular diseases. Int Angiol. 2006 Mar;25(1):4-9. PMID:16520717
Howard BV, Wylie-Rosett J. Sugar and cardiovascular disease: A statement for healthcare professionals from the Committee on Nutrition of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association. Circulation. 2002 Jul 23;106(4):523-7. PMID: 12135957
Elkeles RS. Blood glucose and coronary heart disease. European Heart Journal (2000) 21, 1735–1737 doi:10.1053/euhj.2000.2331
Stanhope KL, Bremer AA, Medici V, et al. Consumption of Fructose and High Fructose Corn Syrup Increase Postprandial Triglycerides, LDL-Cholesterol, and Apolipoprotein-B in Young Men and Women. The Journal of Clinical Endocrinology and Metabolism. 2011;96(10):E1596-E1605.
Shai I et al. Cirulation. 2010; 121:1200-1208
Krauss RM, et al. Prevalence of LDL subclass pattern B as a function of dietary carbohydrate content for each experimental diet before and after weight loss and stabilization with the diets. American Journal of Clinical Nutrition. 2006; 83:1025-1031
Gentile M, Panico S, et al., Clinica Chimica Acta, 2013, Association between small dense LDL and early atherosclerosis in a sample of menopausal women, Department of Clinical Medicine and Surgery, University “Federico II” Medical School, Naples, Italy Division of Cardiology, Moscati Hospital, Aversa, Italy A. Cardarelli Hospital, Naples, Italy

November 7, 2015

PeriScope: How Does Exercise Help Ketosis?

In light of the fact that exercise DOES NOT cause weight loss, exercise has a fascinating ability to enhance ketosis. No, seriously, I don’t care what your trainer told you, you won’t loose weight with exercise, no mater how hard you try. However, exercise does help you body attain a ketogenic state.

When you exercise, the muscles take up glucose and oxygen to burn as their primary fuel. Exercise has actually been shown to enhance this process and reduce the “insulin resistance” effect that the the SAD diet (Standard American Diet) has on 2/3rds of the population (whether they realize it or not). Mild to moderate exercise like a walk or even a mild jog, and resistance training like weight lifting, yoga or Pilates increased the drive of the glucose into the cells and improves the ability of the cells to use the glucose.

In a person following a carbohydrate restricted diet (Ketogenic, Low-Carb, and even Paleolithic to some degree), the body maintains a stable level of blood sugar by releasing glycogen from the liver and gluconeogenisis as needed to support the 100 grams necessary per day required by the brain (the liver makes about 240 grams per day no mater what you do). In the absence of extra glucose as fuel, the body will then use triglyceride and/or ketones as fuel. Exercise improves the sensitivity to the small amount of glucose and actually ramps up the presence of ketones placing the person into a more ketogenic state.

This enhanced ketogensis is often experienced as “second wind” or “being in the zone” or even as an ability to “hyperfocus” during exercise. But the exercise levels must be in the mild to moderate range for this to be accomplished.

But, there’s a fine balance, if the muscles are pushed too hard to fast, lactic acid builds up because of a shift to an anaerobic state and the acid creates a stress response, triggering cortisol and increased glucose formulation, causing one to shift out of ketosis.

How do you know if you exercising too hard? You should be exercising hard enough to break a sweat, but not so hard that you can’t carry on a conversation with your partner at the same time. Over time, as the body becomes more effective at using ketones, you’ll find your exercise intensity can and will improve.

See Dr. Nally try to explain all this while riding his horse Bailey in the White Tank Mountains:

Or you can Katch it here: https://katch.me/docmuscles/v/ce43292a-296f-3de4-bf6f-d19cd688fc62

Have a great weekend!!

October 28, 2015

Red & Processed Meats . . . The Hidden Agenda

I’ve been hearing it all day. Almost every patient asked me the question: Is red meat really as bad as the World Health Organization is claiming? Multiple articles can be found today in the New York Times, and the Washington Post, and even in Money Magazine today. (Money Magazine . . . really?!)

The World Health Organization (WHO) is claiming that processed meats are cancer causing or carcinogenic on the same level as alcohol and asbestos. They also are claiming that red meat is “probably” carcinogenic. “Probably.” That’s a pretty big hedge for a claim of cancer after years of research was reviewed in meta-analysis. Probably is defined by Merriam-Webster to mean: “as far as one can tell.” Well, I can tell you, as far as I can tell, this is bad science being reported as fact to sway the lay mind in following an agenda.

The real story here is NOT that red meat is bad. The real story, that absolutely no one has mentioned, is the veiled agenda cloaked as blame placed on a source of food. This is the WHO’s first step in advancing the Global Warming Agenda.

“Oh, no, Dr. Nally. Here you go talking all that crazy conspiracy stuff!”

No, let me spell it out in the actual words of the World Health Organization.

First, the WHO Director General has published a Six Point Agenda, this year, specifically outlining her vision for high priority issues. The first point on this list of six is to “drive the global agenda . . . in the context of accelerating progress to the Millennium Development Goals.” (1) What in the world are Millennium Development Goals you may ask?

The Millennium Development Goals were first identified in 2000 at the United Nation’s Sustainable Development Conference and reconfirmed this year. These goals specifically outline a transformational vision of the world. The World Health Organization has taken these 16 goals as their “call to arms.” Goals #12 and #13 specifically discuss “ensuring sustainable food consumption patterns throughout the world” by “doubling agricultural growth” and restricting food production that worsens the “carbon footprint.” (2)

Over the last ten years, multiple progressive groups and sites have made the claim that the greatest threat to Climate Change is the cattle industry. They link cattle, livestock and our consumption of red meats to global warming and have been preaching the politics of nutrition. They claim that the only real way to stop climate change and global warming is to “eat less red meat and dairy products.” (3)

The claim is that if we each reduce the red meat in our diet, it will reduce the number of livestock around the world and decrease methane production . . . that causes global warming. I can personally attest to you, that if you eat a more vegetarian diet including cauliflower, broccoli, eggplant and legumes, you alone will increase the methane production in the atmosphere!

In fact, the Lancet, a well recognized medical journal, has published a series of articles yearly, starting in 2008, calling for the reduction in red meat, pork and livestock to control climate change. (Wait a minute? I thought the Lancet was a journal dedicated to diabetes?) All of their climate change/red meat research is based in meta-analysis consisting of “reported” meals by subjects from memory over a 5 year period. Who can remember what they ate last week? These authors then make claims of conjecture, stating that sources of meat “could be,” “may be,” or “probably are” harmful and “have the potential to” reduce climate change (4).

Second, links to cancer using processed meats are very, very small, . . . like a 0.04% chance of colon cancer if you eat processed meats. You have the same chance of getting hit by lightening in your lifetime – 0.04% chance (5). To liken this level of risk in the main stream media to that of smoking or asbestos exposure is immoral and unethical.

Urea Cycle

The concern for many regarding processed meats is the nitrate contents from nitrogen byproducts. About 5% of nitrates are converted into nitrites in the gut, and these can affect the oxidation within the colon an the blood stream. However, most of us handle these nitrites and nitrates through the urea cycle without any problem. Third, spinach, lettuce, cabbage, bok choy and carrots have two to five times higher nitrate concentrations than bacon and hot dogs (6). (Hmmm . . . wonder why the WHO didn’t classify spinach and lettuce as carcinogenic?) Fish produce nitrites in their waste and plants absorb the nitrites in the ponds and lakes and bodies of water they live in. (Look up aquaponics). Most of us have the ability to block the conversion and clear any nitrites out of our systems. The problem arises when we ingest foods that are high in nitrates in conjunction with high fructose corn syrup or “sugar,” to be simplistic. The hepatic (liver) metabolism of fructose in the presence of glucose (that’s what happens when we ingest sugar) inhibits endothelial nitric oxide synthase, increases insulin and suppresses the uric acid cycle allowing for build up of nitrites in the system. It’s the decreased nitric oxide and the high insulin response most of us get from eating the bread or juice with the bacon or the sausage that inhibits our ability to block the conversion leading to carcinogenic levels. (It ain’t the meat . . . its the sugar and the insuiln!!)

As for me, “pass the pastrami, I’m going to sit on the porch and watch a really amazing lightening storm.”

References:

WHO Director General Six Point Agenda, Publications. http://www.who.int/nmh/publications/6point_agenda_en.pdf, October 27, 2015.
United Nations – Sustainable Development Knowledge Platform. Transforming our world: the 2030 Agenda for Sustainable Development. https://sustainabledevelopment.un.org/post2015/transformingourworld, October 27, 2015
Time For Change. Are cows to blame for global warming? Are cattle the true cause for climate change? http://timeforchange.org/are-cows-cause-of-global-warming-meat-methane-CO2. October 27, 2015.
Demaio, Alessandro R et al. The Lancet. Human and planetary health: towards a common language. http://www.thelancet.com/journals/lancet/article/PIIS0140-6736(15)61044-3/fulltext#back-bib10. October 27, 2015.
National Geographic. Flash Facts about Lightening. http://news.nationalgeographic.com/news/2004/06/0623_040623_lightningfacts.html
NG Hord et. al. American Journal of Clinical Nutrition. Food sources of nitrates and nitrites: the physiologic context for potential health benefits. July 2009, Vol 90, 1-10. http://ajcn.nutrition.org/content/90/1/1.full#cited-by. October 27, 2015.

October 17, 2015

Nutritional Values of Brisket . . . on the Fly . . .

My family and I enjoyed some “moist brisket” from Rudy’s Country Store and Barbecue this evening. This is one of my favorite meals. I ordered up 2 lbs knowing that I’d have some to save for later this week. How do you calculate up the ketotic nutritional values for this meal? Easy.

Nutritional values can often be found on the menu or on the web (you might have to ask for it). Rudy’s Country Store kindly places their nutritional information on the web and you can locate it here.

Now, the image above is 2 lbs of moist brisket (with extra bark) and nutritional values are calculated per 1/2 lbs. serving size as noted below. (No, I did not eat this whole thing.) I saved 3/4’s of it for another meal sometime in the next few days.

The Nutritional facts above can be somewhat misleading if you add up the grams of protein, fat and carbohydrate you end up with 93 grams total (the misleading part is that 93 grams does not equal 1/2 lbs. The assumption is that the values are “pre-cooked”). But what I am looking for is the ratio of fat per serving. One serving size has 50 grams of fat and 41 grams of protein. 54% of this brisket is from fat. If you eat the entire 1/2 lbs you’ll go over you protein needs for that meal (assuming that I need only 30-35 grams of protein per meal – 3 meals a day). I only at about 1/3rd lbs. (totally stuffed afterwards) and so 54% of my meal was fat (keeps me in ketosis) and 1/3 lb of the brisket has about 27 grams protein.

Did I calculate all this up before I ate. Absolutely not. I just ate and amazingly, I got full somewhere between 1/4 lb and 1/3 lbs. The key is listen to your body. It will tell you when you are full (unless you are cheating and eating carbs with it, then all bets are off and the satiety signal is delayed).

By the way, it was delicious.

October 13, 2015

How Much #Protein is Too Much on a #Ketogenic Low-Carb Diet? #DocMusclesScopes

How much protein should you be using? Watch the periscope below . . . and good morning from Surprise, Arizona!!

I’ve included the calculations you will need to get a ballpark estimate on your protein intake from your ideal body weight

Ideal Body Weight (IBW):
These calculations are estimated ideal body weight in kilograms (kg). You can convert your weight in pounds (lbs) to kilograms (kg) with the following formula:

The average male needs 1.2 mg/kg protein per day. The average female needs 1.0 mg/kg protein per day.

Males:

IBW = 50 kg + 2.3 kg for each inch over 5 feet.

Females:

IBW = 45.5 kg + 2.3 kg for each inch over 5 feet.

Examples: If I am 6 feet tall, as a male, then I add 50 kg to 27.6 kg ( 6′ tall is 12 inches over 5′ x 2.3 kg) = 77.6 mg of protein requirement per day. That means that if I (a 6′ tall male) ate three times a day, then my protein requirements are 25.9 mg per meal.

October 11, 2015

Low-Carb Maple Pecan Granola . . . (No More Frowney Faces) a DocMuscle’s Favorite

The most exaggerated “frowney” face I get in the office seems to occur when patient’s find out that they cannot eat oatmeal or cereal any longer when following a low-carbohydrate dietary lifestyle. No, oatmeal is NOT good for you . . . I don’t care what WebMD recently said. No, steel-cut oats are even worse (1/4th cup of steel-cut oats is 27 grams of carbohydrate – Who only eats 1/4th cup of oatmeal? Most people eat at least 1/2 -1 cup at a sitting. You do the math . . .)

When I mentioned this to a disabled patient, even her service dog frowned.

Now, before you go running to Larry, the Quaker Oats Mascot (he’s been around for over 140 years), and ask his weight loss advise, I have the solution.

Larry, the Quaker Oats mascot loses 10 lbs for new 2012 cover (He finally figures it out after 137 years)

My angelic wife, Tiffini, the amazing homestead chef and animal husbandry specialist on our little farm, started making low-carb granola for our horseback trail rides. Prior to our discovery of a ketogenic lifestyle, granola was a staple in our pantry, on road trips and in the saddle bags on the trail. This has now replaced any craving either of us had for granola. It carries nicely all day in a Ziplock bag on horseback. It even tastes fantastic in a bowl with unsweetened almond milk as a breakfast alternative if you’re tired of eggs and bacon (but, who ever tires of eggs and bacon? I know . . . Right?!!)

I’ve been nibbling from this actual cookie-sheet of low-carb granola while writing this post. . . I wish you were here to share it with. Soooooo very good, and good for your ketogenic lifestyle. I think I’m going to eat another handful while I finish up Part II of the Principle Based Ketogenic Lifestyle post. Enjoy . . .

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Tiffini’s Maple Pecan Granola (Low-Carb)

1/4 cup butter

1 1/2 cup almonds

1 1/4 cups pecans, divided

1 cup flax seed meal

1/2 cup sunflower seeds – salted

1 cup coconut flakes, unsweetened finely chopped

1/2 cup vanilla whey protein powder – we like ISO-100

1/2 cup pepitas (pumpkin seeds), salted

1/4 cup granulated erythritol

1/8th tsp stevia extract

1 pinch of salt

2 egg whites

1 tsp EZ Sweetz (or 1/2 cup of Sweet Perfection)

1/4 cup Walden Farms Carb Free Maple Syrup

In a food processor, process the almonds and 1 cup of the pecans until it resembles coarse crumbs. Using a knife (preferably a sharp one – remember all bleeding stops eventually), chop the remaining 1/4 pecans coarsely.

Melt the butter and place it in mixing bowel or mixer (We use a Kitchen Aid Mixer). Pour the coarsely chopped nuts into the mixing bowl. Stir in flax seed meal, sunflower seeds, coconut flakes, pepitas and vanilla whey protein powder. Blend in the remaining wet mixture, egg whites and add a pinch of salt. Mix until it forms “clumps.”

Spread the mixture evenly on a large wax paper covered baking or cookie sheet and bake at 350 degrees F for 20-25 minutes or until golden brown. Let it cool on the baking sheet to crisp up for a few hours.

It can be stored in a Ziplock bag in the refrigerator.

Yields 10 servings

1/3rd cup per serving

~ 4 g net carbs

14 g protein

30 g fat

Recipe was modified from Carolyn Ketchum’s Maple Pecan Flax Granola in Low-Carbing Among Friends, Volume – 1, pg. 169, Eureka Publishing, 2011.

October 4, 2015

The Simple Effects of Ponderizing . . . The First Step in a Principle Based Ketogenic Lifestyle

I have found, over time, that happiness in life seems to be the greatest when I strive for balance in the three basic aspects of life: Mind, Body & Spirit. Yes, I am a physician, and I spend the majority of my day applying advise and treatment plans that have been demonstrated to be effective through the tried and true scientific method. However, I know from personal experience, and from working closely with patients for over 15 years, that science alone, does not bring fullness and happiness to life. Truth and learning can be found through study and also by faith. Finding balance and peace physically is important, but finding that balance emotionally and spiritually are often essential. Being able to follow a Ketogenic Lifestyle effectively over the long term (longer than 6 months) actually requires understanding of some basic principles. This is the first in a series of articles regarding The Principle Based Ketogenic Lifestyle.

I treat patients with obesity, one of the most difficult diseases to address in the medical office. I find that just applying diet alone doesn’t always solve the problem. If the patient’s life is out of balance emotionally or spiritually, the stress this causes often halts effective weight loss and metabolic healing. You may disagree with me on political or religious issues, but healing is not about politics nor is it about religious doctrine – it is about understanding where we are, the path forward, and our potential to get there. The mind, body and spirit are deeply interconnected. Often, until we recognize and treat those connections, true healing cannot occur.

The first step in treating any illness, including weight, is recognition of the problem. The Medical Community has recognized Obesity as a disease, but obesity is also a symptom of underlying physical metabolic dysfunction that may be tied to the mind and spirit. Daily journaling is the tool that lets one see if the dysfunction is tied to mind or spirit. I ask my patients to keep a daily food journal. This is very important in looking at the patterns of macro-nutrient intake. But the more powerful effect of journaling allows one to see how food is tied to emotion – mentally and spiritually.

Simply writing down what you eat each day, when you eat it, and how you felt after you at it is actually quite profound. The patterns that emerge are usually seen and identified by the patient long before I ever see them. In fact, patient’s often bring those patterns up before ever showing me their food journals.

I’ve found, in keeping a food journal myself, that combining my journaling with other other daily goals, uplifting thoughts and reminders was even more helpful and powerful. This can be done on paper, a notebook, a planner or even on the computer. (I have a few patients who are accountants or engineers – they bring in complex spread sheets). What is important is daily consistency. It takes about 3-4 weeks of journaling to begin to see patterns.

I have taken the advise of one of the leaders of my church to “ponderize” a scripture, meaningful poetic verse or truth filled quote each week as part of the journaling process. He defined “ponderizing” as the act of pondering and memorizing a scripture or a favorite uplifting poem or verse each week. This is done by writing the verse on a written card or note in a place that you will see it frequently each day during the week. When you see it, read it and ponder it. Just the process of frequently reading it will lead to memorization each week. I have found that reading and pondering a verse 3-4 times a day for a week, lends itself to easy memorization. Each time you read the verse, think about it and ponder it for a moment, then go on with your day. This will give you a brief opportunity to elevate your thoughts each day, and will give you a place your mind can go and think when you don’t have to think. It gives your subconscious mind the ability to solve complex patterns at a higher level.

Said David O. McKay, “Tell me what you think about when you don’t have to think, and I’ll tell you what you are.” “As a man thinketh in his heart, so is he . . . ” (Proverbs 23:7).

For some reason, with all the cares of the day, work, family and the challenges of life, I have fallen out of this habit for some time. When this leader mentioned this process in his comments, I was reminded of the peace and balance I used to feel each week when doing this simple activity. I have recommitted myself to restart this activity and I invite you to do the same. This time to ponder opens your mind and allows you access the deeper worries and fears holding you from what you what to accomplish. It takes great courage to make permanent lifestyle and dietary changes. When someone can’t clearly see what lies ahead, it fills them with fear, doubt or both. But journaling, even in its simplest form, gives a person the ability to resist and then master the patterns that have kept them from change. As Mark Twain said, “Courage is resistance to fear, mastery of fear – not absence of fear.”

Courage is tested when we purse difficult goals, fight against disease with unknown outcomes, or work to regain health. The testing can be painful. Journaling, and ponderizing in the process, gives courage to take small steps, one day at a time. Admitting to, journaling when we fail or make mistakes, fear of failure or feeling unsure actually increases our courage. Being given a week to ponderize an uplifting scripture or verse enhances that courage . Journaling successes and failures empowers us individually. The psychiatrist Carl Jung wrote:

“There appears to be a conscience in mankind which severely punishes the man who does not somehow and at some time, at whatever cost to his pride, cease to defend and assert himself, and instead confess himself fallible and human. Until he can do this, an impenetrable wall shuts him out from the living experience of felling himself a man among men. Here we find a key to the great significance of true unstereotyped confession – a significance known in all the initiation and mystery cults of the ancient world, as is shown by a saying from the Greek mysteries: ‘Give up what thou hast, and thou will receive.'”

Journaling and ponderizing allows one a form of confession and renewal. It gives one courage that you have survived today’s challenges and seen the pattern of fallibility in them. It is actually energizing. And, the path to healing begins to become clear.

Journaling also is a great way to outline side effects from carbohydrate withdrawl that will last for 2-4 weeks (That’s for another blog post, however).

Feel free to ask me about the verse that I am ponderizing each week. I will happily tell you which verse I am pondering and memorizing; but, I will in tern, ask you which verse you are ponderizing.

This week, the verse I am ponderizing comes from the Bible – Genesis 35:2-3:

“Then Jacob said unto his household, and to all that were with him, Put away the strange gods that are among you, and be clean, and change your garments: And let us arise, and go up to Beth-el; and I will make there an altar unto God, who answered me in the day of my distress, and was with me in the way which I went.”

Did you begin your food journal? And, what verse are you going to ponderize this week?

September 30, 2015

Cinnamon Swirl Cheese Cake . . . (I think this will be a desert on the menu in Heaven)

While at the house last night, Jimmy Moore, his wife Christine, and my wife Tiffini made this delicious cinnamon swirl cheese cake from The Ketogenic Cookbook. I think I have a new favorite!!! I seriously have not had a better cheesecake and this one is lowcarb, gluten free and keeps you in ketosis. Thank you Jimmy Moore and Maria Emmerich for such a yummy recipe. (I even had some for breakfast this morning . . . . mmmmm).

If you want a great low carb recipe, pick up a copy of the book and turn to page 336.

Until next time . . . keep the ketones high!

September 21, 2015

Homemade Rootbeer – Ketosis Style!!

ery October I get a hankering for homemade root beer. But it is usually loaded with sugar. Thanks to Maria Emmerich and her amazing recipes, that doesn’t have to happen this year. She just posted this on her site today and I can’t wait to try this as I sit by my fire pit roasting some hot dogs with my kids . . . Thanks Maria.

I pasted a copy of her root beer image below just to make you drool, too . . .

Link on the recipe at her site HERE.

(Another great use for the SodaStream as well . . . the day just keeps getting better!)

September 10, 2015

The Dreaded Seven . . . (Seven Detrimental Things Caused by High Insulin Loads)

85% of the people that walk through my office doors have some degree of insulin resistance.

What is “insulin resistance?” It is an over production of insulin in response to ANY form of carbohydrate intake (yes, even the “good carbs” cause an insulin over-response in a person with insulin resistance.)

How do I know this? Because I routinely check insulin levels (I check them every three months) and the down stream markers of insulin on a large number of the patients that I see. I have been fascinated by the fact that a diet high in both sugar and fat [like the Standard American Diet, (SAD) diet] turn on the genetics leading to insulin resistance. Starch and sugar load the genetic gun.

Insulin acts like a key at the glucose doorway of every cell in your body. In many people, the insulin signal is blocked by hormones produced in the fat cell and the the insulin, acting like a “dull or worn out key” – can’t open the glucose doorway as efficiently.

So, the body panics, and releases extra insulin in response to the same load of carbohydrate or glucose. People with insulin resistance will produce between 2-20 times the normal amount of insulin in response to a simple carbohydrate load. Recent studies(1, 2) reveal high cholesterol and diets high in both fat and carbohydrate cause insulin resistance to progress or worsen.

So, instead of producing enough insulin to accommodate the one slice of bread or the one apple that you might eat, the insulin resistant person produces enough insulin for an entire loaf of bread or an entire bushel of apples. This excess insulin then stimulates one or all of the following:

Weight Gain – Insulin directly stimulates weight gain by activating lipoprotein lipase to take up triglycerides into the fat cells. This causes direct storage of fat and increases your waistline. (3)
Elevated Triglycerides – Insulin directly stimulates production of free fatty acids and triglycerides through hepatic gluconeogenesis and is even more notably amplified by the broken signaling mechanism of the FOX-01 phosphorylation mechanism in patients with insulin resistance. (4)
Increased number of Small Dense LDL (sdLDL) particles – Low density lipoprotein (LDL, or “bad cholesterol”) is actually comprised of various sized lipoproteins including small, medium and large. As triglycerides increase, the small dense LDL particle numbers increase. Research points to the fact that it is the small dense particle that is highly atherogenic (leading to the formation of vascular plaques within the arteries). (5, 8)
Elevated Uric Acid – Leptin resistance and insulin resistance syndromes are often found together and are suspected to have significant influence on each other. High insulin loads lead to “sick adipose cells” causing leptin resistance. This has a dramatic effect on hepatic fructose metabolism increasing the production of uric acid. Excess insulin suppresses urinary excretion of uric acid and dramatically increases serum content of uric acid and the risk of kidney stones and gout. (6, 7)
Increased Inflammation – Increased levels of circulating insulin have a direct correlation on raising many of the inflammatory markers and hormones including TNF-alpha and IL-6 in the body (9). Any disease process that is caused by chronic inflammation can be amplified by increased circulating levels of insulin including asthma, acne, eczema, psoriasis, arthritis, inflammatory bowel and celiac disease, etc.
Elevated Blood Pressure – Increased uric acid production from insulin resistance as noted above directly suppresses production of nitric oxide within the vasculature and increases blood pressure (7). This completes the triad of metabolic syndrome (elevated triglycerides & cholesterol, weight gain, and elevated blood pressure) found in patients with insulin resistance.
Water Retention – We have known for many years that insulin affects the way the kidney uses sodium in the distal nephron. Insulin has a direct effect on sodium retention in the kidney. As insulin levels rise, the kidney retains increased levels of sodium (10). Water follows sodium and thereby causes fluid retention. This is the reason that many of my insulin resistant patients who have struggled with leg swelling and edema suddenly improve when they correct their diet and their high circulating insulin levels fall. It is also the reason that many of my patients show up in my office after the holidays with swollen legs and amplified swelling in their varicose veins after cheating on their ketogenic diets.

If you are plagued by any or all of these, my first suggestion is to see your doctor and get screened for insulin resistance. I treat patients with these every day and have reversed these effects in thousands of patients with the correct diet and/or medications. Having seen these signs and patterns over the last 20 years of medical practice, I am still astonished every day by the dramatic effect our diet plays on the hormonal changes within the body. Remember that the food you eat is actually the most powerful form of medicine . . . and the slowest form of pernicious poison.

A ketogenic or carnivorous diet is your first step.

We take most insurances, however, check out my concierge program or my Direct Primary Care program if you are interested in an alternative to insurance.

References:

Cholesterol Elevation Impairs Glucose-Stimulated Ca2+Signaling in Mouse Pancreatic β-Cells, Endocrinology, June 2011, Andy K. Lee, Valerie Yeung-Yam-Wah, Frederick W. Tse, and Amy Tse; DOI: http://dx.doi.org/10.1210/en.2011-0124
Glucose-Stimulated Upregulation of GLUT2 Gene Is Mediated by Sterol Response Element–Binding Protein-1c in the Hepatocytes, DIABETES, VOL. 54, JUNE 2005; Seung-Soon Im, Seung-Youn Kang, So-Youn Kim, Ha-il Kim, Jae-Woo Kim, Kyung-Sup Kim and Yong-Ho Ahn
Obesity and Insulin Resistance. J Clin Invest. 2000 Aug;106(4):473-81.Kahn BB, Flier JS
Selective versus Total Insulin Resistance: A Pathogenic Paradox, Cell Metabolism, Volume 7, Issue 2, 6 February 2008, Pages 95–96, Michael S. Brown, Joseph L. Goldstein
Association between small dense LDL and early atherosclerosis in a sample of menopausal women, Department of Clinical Medicine and Surgery, University “Federico II” Medical School, Naples, Italy Division of Cardiology, Moscati Hospital, Aversa, Italy A. Cardarelli Hospital, Naples, Italy, Gentile M, Panico S, et al., Clinica Chimica Acta, 2013
Sugar, Uric Acid and the Etiology of Diabetes and Obesity. Diabetes. 2013;62(10):3307-3315, Richard J. Johnson; Takahiko Nakagawa; L. Gabriela Sanchez-Lozada; Mohamed Shafiu; Shikha Sundaram; Myphuong Le; Takuji Ishimoto; Yuri Y. Sautin; Miguel A. Lanaspa
Fructose: metabolic, hedonic, and societal parallels with ethanol. J Am Diet Assoc. 2010 Sep;110(9):1307-21. doi: 10.1016/j.jada.2010.06.008. Lustig RH
Cardiovascular Risk in Patients Achieving Low-Density Lipoprotein Cholesterol and Particle Targets. Atherosclerosis. Vol 235; 585-591, May 2014, Peter P. Toth, Michael Grabner, Rajeshwari S. Punekar, Ralph A. QuimboMark J. Cziraky c, Terry A. Jacobson
Chronic Subclinical Inflammation as Part of the Insulin Resistance Syndrome The Insulin Resistance Atherosclerosis Study (IRAS), Circulation, July 2000, 102:42-47; Andreas Festa, MD; Ralph D’Agostino, Jr, PhD; George Howard, DrPH; Leena Mykka¨nen, MD, PhD; Russell P. Tracy, PhD; Steven M. Haffner, MD
The Effect of Insulin on Renal Sodium Metabolism. Diabetologia. September 1981, Volume 21, Issue 3, pp 165-171. R. A. DeFronzo

September 8, 2015

Snack Time . . . Bacon Chips & Guacamole!!

To maintain ketosis, the key is keeping the fat content high and the carb content low . . .while moderating the protein intake. Unless you are running triathalon’s, body building daily or exercising more than 45 minutes daily, most women don’t need more than 70-80 grams of protein per day. Most men don’t need more than 80-90 grams per day.

Now, stop looking at your phone and go make some bacon chips . . . 🙂