Statin drugs have been show to increase risk of death with a COVID-19 infection.
Tag: Diabetes Mellitus
Why Salt is So Important on a Ketogenic Diet?
The most common complaint that I get in my office when someone has started a ketogenic diet is, “Doc, I feel fatigued. Will this ever go away?”
That feeling of fatigue, some refer to as the “keto-flu,” is usually due to a couple of things. First, you may not be eating enough fat (I recommend a 1 gram to 1 gram ratio of protein to fat when getting started). Second, you’re not taking in enough salt (specifically sodium, potassium, magnesium and/or zinc). These four salts are essential electrolytes our body requires for proper function.
If salt is the problem, the you will be experiencing leg cramps. Cramps during daytime activity are usually due to low sodium or potassium levels. Cramps that wake you up at night are usually due to low magnesium or zinc. Leg cramps can also be due to hypothyroidism or significant blood sugar swings. Dr. Nally will usually check for this during your visit with him.
“But isn’t too much salt bad for you?” I am frequently asked.
Too much salt is only bad for you if you’re eating a “low-fat” diet.
What if increasing salt intake actually lowered your blood pressure?
Did you know that increasing your salt intake can actually improve your diabetic blood sugar if you are following a correct diet? Could it be that easy?
Almost every patient that I see in the office has a significant worry about salt intake, some greater than others. In fact, some people are so fearful about salt that when I initially began encouraging its use, they told me that I was crazy, and they left my practice.
Has restricting salt over the last 50 years really worked, or is it doing more damage than we think?
That was the question that was asked by Dr. Ames in the American Journal of Hypertension 17 years ago. However, his answer never got a mention. In fact, I’ve been in practice for almost 20 years, and incidentally stumbled upon this article when it was mentioned by a colleague of mine. Granted, the study is a small sample size of people, only twenty-one. However, the results are profound.
Twenty-one patients with hypertension were randomized to periods of no salt (placebo) and periods of 2 grams (2000 mg) of sodium chloride four times a day (a total of 8 grams of salt per day). Glucose tolerance tests were completed with insulin levels at the end of each intervention period.
Insulin Resistance and Hypertension Improve by Adding Salt
Three very noteworthy results happened. First, those patients with insulin resistance and diabetes had improvement in their glucose levels while on 2 grams of sodium supplementation.
Second, those with hypertension also, shockingly, showed improvement in their blood pressure while on the 2 grams of sodium supplementation.
Third, those with insulin resistance had a lowering of their insulin levels during the period of increased sodium intake. These findings fly in the face of the dogma that’s been drilled into our heads that “salt is bad!”
“But, Dr. Nally, you can’t base your findings on a small group of 21 people,” the experts say.
Yes, it is a small study group. However, these findings are identical to what I, also, see clinically every day in my practice for over 20 years.
We know that the average human needs at a minimum 3 grams of sodium per day and 3 grams of potassium per day. The standard American diet (SAD diet) including processed foods contains 2-3 grams per day of sodium and potassium. In fact, the CDC claims the worst salt containing meals for you are:
- Bread
- Processed chicken dinners
- Pizza
- Pasta
Insulin also stimulates additional retention of sodium at the kidney level. If you are insulin resistant, producing excess insulin in response to starches or sugars, you retain notably larger amounts of salt when eating the standard American diet (SAD diet) or a “low-fat” diet. However, if your following a low-carbohydrate or ketogenic lifestyle, you won’t be eating the meals above and you’re probably not getting near enough salt.
Salts, or electrolytes, are essential in normal cellular function. Low salt in the body is like running your car without oil. It will run, but not very efficiently and over the long term will cause problems. This is the cause of the keto-flu I wrote about previously. And, according to the study above, it is a potential driver of our persisting insulin resistance, diabetes and hypertension.
How Much Salt Should I Use?
In my office, I encourage use of 3-4 grams of sodium and 3-4 grams of potassium daily when using a ketogenic lifestyle. That’s approximately 1 ½ – 2 teaspoons of salt per day. I like the Redmond’s RealSalt or pink Himalayan salt because these products contains all four types of salt (sodium, potassium, magnesium and zinc).
It is probably that your salt restrictions is making your insulin resistance and blood pressure worse. That’s what the clinical evidences are pointing toward, and it is what I see every day in my office.
Want to know more about a ketogenic life-style? Click the KetoLife link to get some basics.
If you’re already following a ketogenic lifestyle, then let me help you navigate the bumps and turns by going to the KetoKart and checking out the products I recommend to jump-start ketosis DocMuscles-style!
Until then, I’ll have another piece of bacon, please . . . and, oh, pass the salt!
Ketones – One of the Keys to the Fat Lock-Box
Do you have the keys to your “fat lock-box?”
Lock-boxes have always fascinated me. Lock-boxes with special keys are even more fascinating. The more I’ve learned about fat cells (adipocytes), the more I think about them as special fuel depositories or fat lock-boxes. Before the invention of refrigerators, fast-food, Bisquick and beer, our bodies preserved and reserved fat as a precious commodity.
The body, when given fat with carbohydrates or excess protein, quickly places the fat into a lock-box for safe keeping. It does this for two reasons. First, the body can store fat very efficiently. Second, hormone signals stimulate fat storage when other fuel sources (carbohydrate & protein) are present in excess. The body can access this stored fuel only when the right presentation of hormonal keys are present. Fascinatingly, we now know from recent research, there are actually three types of lock-boxes for fat in the human body (white adipose tissue, brown adipose tissue, and tan adipose tissue).
The greatest challenge for the obesity doctor is getting into the fat lock-box. Some people’s boxes are like the “Jack-in-the-Box” you had as a child – just add a little exercise spinning the handle and the box pops open (These are those people that say, “Oh, just eat less and exercise and you’ll lose weight.”) For the majority of the people I see, it’s more like the lock above with a four or five part key required to turn the gears just right. (And, that key often only seems available on a quarter moon at midnight when the temperature is 72 degrees.) Fat cells, called adipocytes, require four, and possibly more, keys to open them up and access the fuel inside. Exercise is only one of those keys. However, exercise alone often fails.
Over the last 18 months, I have been surprisingly impressed with the results patients have by the addition of both medium chain triglycerides and exogenous ketones. A number of people have asked me, “Why do you encourage the addition of exogenous ketones to a person already following a ketogenic diet?”
Others just accuse me of self promotion, saying, “You’re just trying to sell a product!”
Or they exclaim, “Giving more ketones is just a waste of time and money.”
A few of the uneducated holler from across cyberspace, “You’re just going to cause ketoacidosis!”
Believe me, I’ve heard it all. And, the skepticism is understandable. I work with people every day, looking closely at weight gain/loss, metabolism, cholesterol, blood pressure, inflammation, etc. With any “low-carb” or “ketogenic product,” I test it out on myself and my family, before I offer it to my patients or even consider encouraging its use in my practice. I have this desire to understand “the how” and “the why” before I prescribe the who and when.
The Fat Lock-Box Keys
First , let’s talk about the adipocyte as a fat lock-box – and where you find the keys. Then, we’ll discuss how products may or may not help.
Insulin
There is only one door INTO the adipocyte for the fat, and the key to that door is insulin. Insulin stimulates an enzyme called lipoprotein lipase that essentially pulls the fat from the cholesterol molecule into the fat cell. Without insulin, fat doesn’t enter the fat cell. As a result, type I diabetics (those that make absolutely no insulin) look anorexic if they don’t take their needed insulin. Insulin is also the first key to the back door on the adipocyte. Actually, if there is too much insulin in the system, fat enters easily through the front door but cannot exit the back door (Picture 1). Insulin seals up the back door so that fat cannot exit very effectively.
That’s why insulin is the master hormone when it comes to obesity. You’ve got to lower the over-all insulin load to get the adipocyte slowing fat entry and increasing fat exit. If you don’t do that, I don’t care how much you exercise, 85% of the population will struggle with weight loss. Hmmm, seems kind a familiar to the last 50 years of our obesity epidemic, No?
Catecholamines
The second key to the back door of the fat cells are the catecholamines. These are adrenaline (epinephrine), norepinephrine, adrenocorticotropic hormone (ACTH) and even serotonin. These hormones are produced in the adrenal glands through exercise, fear and even recollection of powerful memories. Medications can also stimulate production of these hormones. The catecholamines stimulate cAMP. cAMP opens the fat cell, releasing fatty acids for fuel.
The thyroid hormone conversion of T4 to T3 also plays a role in uptake of the catecholamines by adnylyl cyclase (AC). Low levels of T3 (like those seen in hypothyroidism or in cases of thyroiditis) also inhibit unlocking of the fat lock-box. Conversion of T4 to T3 is driven by the presence of bile salts in the gut. Increase fat intake increases the presence of the bile salts which naturally leads to better T3 conversion. Hence my constant references to eating more fat and bacon. .
Inflammation & Medications
The third key is an inhibitory effect on adenylyl cyclase (AC) activity by alpha and beta adrenoreceptors, adenosine, prostaglandins, neuropeptide Y, peptide YY, HM74-R & nicotinic acid. These inhibitory and inflammatory hormones produced in the brain, gut and other areas decrease cAMP activity in the fat cell and slow fat loss. The fancy long names are all hormones causing inflammation. Of note, many are also stimulated by medications including blood pressure lowering drugs. Check with your doctor if the medications you are taking may be causing weight gain, or halting your weight loss.
Please note that the first three keys have effect on the cAMP pathway for release of fat from the adipocyte. These three keys turn on or off effective function of cAMP leading release of fatty acids from the fat cell.
Naturitic Peptides
The fourth key follows a separate pathway. This is why I’ve clinically seen patients experience weight loss even in the presence of higher insulin, inflammatory disease or hypothyroidism. This key activates release of the naturitic peptides (ANP, BNP). These hormones are released from the heart when it squeezes more powerfully. As the cardiac muscle contracts, it releases ANP & BNP hormones. These hormones stimulate the cGMP pathway in the adipocyte. It then activates hormone sensitive lipase (HSL) and perilipin to release free fatty acids. Again, this pathway is separate from the pathway by which the first three keys released fat. Exercise increases heart contractility, but is inhibited by high insulin levels. However, ketones themselves also stimulate this increased contractile effect.
Hypothalamus-Pituitary-Gonadal (HPG) Axis & Testosterone
There actually is a fifth key not referenced above. The fifth key to the fat lock-box amplifies testosterone’s presence through the HPG axis. Insulin resistance and leptin resistance lower testosterone in men and raise it in women, causing poly-cystic ovarian syndrome (PCOS). Normalizing insulin levels (with a ketogenic diet) while at the same time increasing ketones as the primary fuel powerfully resets the HPG axis through a complex series of hormonal reactions. Growth hormone is balanced and testosterone returns to a normal range.
Clinically, 60% of the people I see in the office have abnormal testosterone due to insulin resistance. This leads to hypogonadism in men and PCOS (abnormal periods, facial hair growth and/or infertility) in women. Restricting carbohydrates and maintaining nutritional ketosis by diet and/or addition of exogenous ketones has a powerful corrective factor in these people.
Testosterone influences the up-regulation of the alpha & beta adrenergic receptors (the 2nd & 3rd key above). Hence, if your testosterone is low, it has a suppression on the way that the catecholamines influence fatty acid release from the fat cells. If your testosterone and growth hormone are normal, muscle development and adrenaline stimulus from exercise helps amplify the use and mobilization of fat from the fat cell. In people with insulin resistance and leptin resistance, exercise and the catecholamines don’t have the same fat burning effect.
What Does This Actually Mean?
Yes, I have greatly simplified a series of very complex hormonal pathways in the explanation of the keys above. Why do you think understanding obesity has been so difficult? Think of your adipocytes as a fat lock-box.
What’s even more important is the knowledge that the fat cell DOES NOT open or close because of calories. There is no dogmatic calorie-meter on the wall of the fat cell. There is no calorie key to the fat lock-box. Really, . . . in the 50 years of studying fat, researchers haven’t found one. (Prove me wrong when you show me an electron micro-graph of a calorie-meter in the wall of a cell). Science has demonstrated multiple times that the lack of food from starvation or excessive fasting suppresses thyroid function (an inhibitory effect on key #3). Restricting calories actually inhibits fat loss in many people.
The fat lock-box keys I refer to above are hormone responses to the presence of macro-nutrients (food). That means, first reduce your carbohydrate intake by eating real food from good sources. You can learn how to get started by registering for my FREE six part weight loss mini-course. Second, be as active as you can. Third, reduce stress and medications that have inhibitory effect on catacholamines. Fourth, balance your thyroid. And, fifth, get into ketosis and consider adding exogenous ketones to your dietary regimen. It really is that simple.
References
(For those of you that still believe there is a calorie key – or just need something to do while in the bathroom):
- Lafontan et al. Arterioscler Thromb Vasc Biol. 2005
- Lenard NR, Obesity, 2008
- Li XF et al, Endo (April 2004) Vol 145
- Liu YY& Brent GA, Trends Endocrinol Metab. 2010 Mar; 21(3): 166–173
- Max Lafontan et al. Arterioscler Thromb Vasc Biol. 2005;25:2032-2042
- Skorupskaite K et al, Hum Rep Update, Mar 2014, vol 20
Fatty Liver Disease – It Isn't Caused By Fat . . .
Two out of ten people that he sees in his office have signs of fatty liver disease. What does that mean to society and how does it affect you?
Spend 11 minutes with Dr. Nally as he discusses the cause of Fatty Liver Disease and discusses the most effective method he has found to treat it. What is the underlying cause? Watch and find out.
Ketogenic Interview with Vicki Fitch: A Fresh Perspective
I had the chance to appear for an interview on Vicki Fitch’s podcast last night: A Fresh Perspective. We talked about bacon, ketogenic diets, hypoglycemia, sweeteners, food cravings, #FitchSlaps, exogenous ketones and we answered a bunch of great questions from the Facebook Live audience. You can see video of the show below:
Had a great time. Let me know what you think. Thanks, Vicki!!
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).
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.
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.
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 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?
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:
- Lane JD, Barkauskas CE Surwit RS, Feinglos MN, Caffeine Impairs Glucose Metabolism in Type II Diabetes, Diabetes Care August 2004 vol. 27 no. 8 2047-2048; doi:10.2337/diacare.27.8.204
- Jankelson OM, Beaser SB, Howard FM, Mayer J: Effect of coffee on glucose tolerance and circulating insulin in men with maturity-onset diabetes. Lancet 1: 527–529, 1967
- Graham TE, Sathasivam P, Rowland M, Marko N, Greer F, Battram D: Caffeine ingestion elevates plasma insulin response in humans during an oral glucose tolerance test. Can J Physiol Pharmacol 79:559–565, 2001
- Greer F, Hudson R, Ross R, Graham T: Caffeine ingestion decreases glucose disposal during a hyperinsulinemic-euglycemic clamp in sedentary humans.Diabetes 50:2349–2354, 2001
- Keijzers GB, De Galan BE, Tack CJ, Smits P: Caffeine can decrease insulin sensitivity in humans. Diabetes Care 25:364–369, 2002
- Petrie HJ, et al. Caffeine ingestion increases the insulin response to an oral-glucose-tolerance test in obese men before and after weight loss. American Society for Clinical Nutrition. 80:22-28, 2004
- Evans SM, Griffiths RR, Caffeine Withdrawal: A Parametric Analysis of Caffeine Dosing Conditions, JPET April 1, 1999 vol. 289no. 1 285-294
- Noever R, Cronise J, Relwani RA. Using spider-web patterns to determine toxicity. NASA Tech Briefs April 29,1995. 19(4):82. Published in New Scientist magazine, 29 April 1995
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 . . .
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 . . .
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.
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!!!
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).
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
Reversal of Diabetes in the Ketogenic Zone – A Case Report
This week I had the pleasure of seeing a really nice 46 year old Hispanic male who is fairly new to the office. He came back in to see me in follow up on his diabetes. To give you a bit of background history, the patient came to see me about 6 months ago, just not feeling very well. Based on his symptoms of fatigue, history of elevated blood sugar and family history, lab work was completed.He saw us initially with a Hemoglobin A1c of 12.3% in June (normal should be 4.9%-5.6%). This means he had an average blood sugar over the previous three months of about 310 mg/dL (normal should be < 110 mg/dL).
Past Medical History include: Diabetes Mellitus – type II (not on any medications when initially seen), Hypertension (high blood pressure), Dyslipidemia (elevated cholesterol) and a non-specific heart arrhythmia.
Medications: None
Surgeries: Knee & shoulder arthroscopies
Family History: Father Diabetes, Stroke, Heart Disease, Hypertension, Elevated Cholesterol
Social History: Non-Smoker, Limited Alcohol Use
He related to me that he had been on metformin before, however, had some significant diarrhea and was not interested in using this medication EVER again. A previous doctor had tried Victoza© (liraglutide), a GLP-1 inhibitor, but he didn’t use it for very long as he didn’t really see much change with this medication.
After getting his labs back, we had a very long conversation about the need to either fix his diet dramatically, or he may be looking at using 3-4 oral medications or even insulin to control his blood sugar.
When I see average blood sugars (HbA1c) stay over 6.5% (or greater than 140 mg/dL), the risk for retinal, kidney and nerve damage is significant and often irreversible after 4-5 years. Most physican’s are affraid to lower the HbA1c to less than 7.0% with medications due to low blood sugar events, and so the diabetes community has “settled” with 7.0% as being effective. However, it still isn’t low enough. I saw this happen with my father and with other members of me family. I’ve seen it happen over and over with my patients over the last 15 years when they have not lowered their blood sugar and reduced the high insulin loads that occur in response to those high blood sugar levels. It has been my experience that HbA1c can be very safely lowered to the normal range, as low as 5.2-5.6% without symptomatic low blood sugars, with the correct diet and careful use of medications.
So, my patient, above, committed to change. I was worried that diet alone would not be able to lower these levels enough to be effective so we discussed tight carbohydrate restriction, the addition of methlyated folate and chromium and a re-trial of a low dose of Victoza© (liraglutide), which he had at home.
I didn’t see him for about three months. When he followed up this week I was amazed. I was amazed because I rarely see more than 1.5% drop in HbA1c with the addition of Victoza© (liraglutide). The additional 4.5% of drop with diet was dramatically impressive.
When we talked, he told me that all he has done differently is use the Victoza© (liraglutide) and cut his carbohydrate intake to less than 10 grams per meal (Yes, he did admit to occasionally cheating).
You can see the dramatic results:
June 2015 |
September 2015 |
|
Glucose |
258 |
103 |
HbA1c |
12.3% |
6.3% |
Urine Creatinine (Random) |
208 |
72 |
|
|
||
Total Cholesterol (mg/dL) |
219 |
218 |
Triglycerides (mg/dL) |
137 |
117 |
HDL-C (mg/dL) |
38 |
37 |
LDL-C (mg/dL) |
154 |
158 |
LDL-P (nmol/L) |
2172 |
1691 |
Small dense LDL-P (nmol/L) |
1289 |
419 |
|
|
||
TSH (mU/L) |
1.75 |
|
|
|
As you can see, a dramatic change in his blood sugar has occurred in a three month interval. Not only that, we see a significant change in his cholesterol profile.
Some might argue that this is the Victoza© (liraglutide) doing this. I can tell you, in the 15 years I’ve been doing this and in the 5 years that Victoza© (liraglutide) has been available in the U.S., I have never seen a drug reduce blood sugar or cholesterol this dramatically.
Previously, we looked at LDL-C for heart disease risk, however, I have multiple patients that have had heart disease with normal LDL-C ( <100 mg/dL). LDL-C is just a summation of all the particles. The LDL particle is actually made up of three sub-types and it is specifically the small dense particle that causes the vascular risk. You can see a dramatic normalization of the small dense particle LDL with no change in LDL-C and minimal change in Total Cholesterol in the patient’s labs when he reduces his carbohydrate intake. This is a pattern I see every single day. When serial carotid ultrasound studies are completed, I see reduction in blockage and reduction in the vascular wall thickening. I will be very interested to see the vascular studies on this patient and I will await his results as he tightens up his diet even further.
All in all, he has dramatically brought his diabetes under control with carbohydrate restriction and if he continues this lifestyle, he has reduced his risk for retinal damage, reduced his risk for kidney damage, reduced his risk for nerve damage and essentially added 20 years to his life.
(Disclosures: Dr. Nally has no vested interest, monitary or otherwise, in Novo Nordisc or it’s products including liraglutide.)
Fructose and High Triglycerides Lead to Leptin Resistance
I can’t help myself. Some days I enjoy a good murder mystery, but on others, I enjoy a good journal article elucidating our understanding of leptin. No, leptin is not a tiny Irish folk character or even a superhero. Leptin is a hormone. It’s made by fat cells. Anything made by fat cells becomes fascinating to a “fat doctor.”
Why is learning about leptin illuminating?
Well, if Sir Arthur Conan Doyle was an Obesity Specialist, the mystery would have been that Mr. Plump was killed by the wrench in the kitchen, but the wrench seems to have never left tool case in the garage. No one has been able to figure out how leptin, the allegorical wrench, plays its roll in lepin resistance. We know that a lack of leptin allows hunger to persist and a person without leptin will continue to eat without the sensation of feeling full – leading to obesity. What we haven’t understood is – what causes the brain to no longer sense larger and larger amounts of leptin being produced by those who are obese.
That is . . . we haven’t understood it until now. . .
We have known for some time that the hormone leptin is a key hormone produced by the adipose (fat) cells that suppresses hunger. A majority of obese patients in my clinic have elevated circulating leptin levels 2-10 times the normal levels. We know that a lack of leptin leads to obesity, but the patients that I see in the office are producing an over abundance consistent with leptin resistance. The leptin signal is not being recognized by the brain. This is very similar to type II diabetes and insulin resistance. The pancreas is producing an over abundance of insulin, but the cells are recognizing the signal to let the glucose in through the door way.
Three recent and very interesting studies have pointed to the probable cause. First, one of the most common genetic disorders causing human obesity is loss of function of the melanocortin receptor.
If the MC-4R receptor is broken, suppression of appetite is limited, continued eating occurs and weight gain continues. Leptin, produced by every adipose cell in the body, is carried in the blood stream to the brain and must pass through the blood-brain barrier. Once it crosses the blood-brain barrier and enters the hypothalamus, it has a stimulatory effect on the MC-3R receptor in the Arcuate Nucleus of the hypothalamus causing stimulation of the MC-4R receptor in the Parventricular Nucleus and Lateral Hypothalamus to turn off hunger.
However, if leptin cannot cross the blood brain barrier, the signal is never received from the adipose cells and continued eating without satiation (feeling full) persists. Studies have shown that dietary fructose ingestion alone or in combination with diets high in fat suppress the transmission of leptin across the blood-brain barrier.
Fructose is the primary component of high-fructose corn syrup, and makes up 45-50% of every other type of natural form of sugar (sucrose). Yes, it’s the major component found in table sugar, brown sugar, honey, agave, molasses and maple syrup. This is why a Paleolithic Diet isn’t fully effective for people with leptin resistance.
Lastly, anything that raises triglycerides inhibits leptin from crossing the blood-brain barrier.
Insulin has a direct effect on triglycerides. (See the articles “Insulin Resistance & The Horse,” “Fat Thoughts on Cholesterol,” “Ketogenic Living” and “So, What is this Ketogenic Thing?“). If your insulin levels go up, triglyceride production goes up. The patient with insulin resistance, pre-diabetes, impaired fasting glucose or type II diabetes produces between two to ten times the normal amount of insulin when eating the standard American diet (SAD diet). These patients have significant triglyceride elevation because of the high insulin response to carbohydrates in their diet. (Many of them were told by their doctor that “It’s just genetic so take your Lipitor.”) Statin drugs lower the LDL-C (calculated “bad cholesterol” level), but don’t reduce triglycerides effectively. Inadequate treatment of high triglycerides allows poor blood-brain barrier transmission of leptin and worsening leptin resistance.
In fact, this is the challenge and problem with the “frequent fasting” or “intermittent fasting” fad for weight loss that has been popping up in the blogosphere. If fasting reaches a state of starvation (which is a very fine line metabolically), it stimulates a stress response . . . causing a spike in cortisol, release of glycogen (a form of sugar), a compensatory release of insulin and a spike in triglycerides. If you have tried intermittent fasting and you’ve gained weight, you are probably not “fasting,” your probably “starving.” We’ve known for years that triglycerides are elevated in starvation. This diminishes leptin’s ability to cross the blood-brain barrier and leads to worsening leptin and insulin resistance.
High leptin levels caused by leptin resistance also seems to play a significant role in the development of diabetic retinopathy – damage to the tiny blood vessels at the back of the eye feeding the retina. Diabetic retinopathy starts insidiously without any symptoms initially and can lead to eventual blindness if not treated. Leptin seems to upregulate vascular endothelial growth factor (VEGF) which leads to narrowing of the blood vessels called “ischemia.” Chronic ischemia of the retinal vessels leads to damage to the delicate retinal cells of the eye.
So what do you do if you have leptin resistance. First, eliminate carbohydrates from your diet, especially sugars, high fructose corn syrup and any other form of simple sugar. This is why I am such a big fan of low carbohydrate, high fat diets.
Second, lower your triglycerides. This is done through decreasing overall insulin loads and is very effectively accomplished with a ketogenic diet. You can find this in my book, The KetoCure. Some additional great sources are KetoClarity, The Art and Science of Low Carbohydrate Living, and The Ketogenic Cookbook.
Third, use a supplement containing alpha-lipoic acid, carnosine high gamma vitamin E and benfothiamin (derivative of Vitamin B1). These have been demonstrated to decrease inflammation and render protection to the blood vessels.
The use of Epigallocatechin gallate (EGCg), a derivative extract of green tea, has been shown to repress hepatic glucose production, one of the insidious factors of insulin resistance, and may play a role in stabilizing the effect insulin has on production of triglycerides. You should consider using KetoEssentials. It is my specially formulated multivitamin that contains all of the above supplements, and includes methylated folic acid (B9), the necessary vitamin B6 & B12, chromium, vandium & zinc that help to further stabilize insulin resistance.
Fourth, get a good night’s sleep. Lack of sleep causes a stress response, increases cortisol, raises blood sugar and insulin leading to further leptin resistance.
Fifth, mild to moderate resistance exercise has been shown for years to improve insulin resistance significantly. If you’re not exercising, take a 20 minute walk 2-3 times per week, ride a bike for 20 minutes, start a weight lifting program, consider yoga or Pilates, Remember, jumping to conclusions, flying off the handle, carrying things too far, dodging responsibility and pushing your luck don’t qualify as resistance exercise.
Above all, if you’re having trouble losing weight, controlling insulin or leptin, see your doctor. He or she can really help.
References:
- Ray F. Gariano, Anjali K. Nath, Donald J. D’Amico, Thomas Lee, and M. Rocio Sierra–Honigmann. “Elevation of Vitreous Leptin in Diabetic Retinopathy and Retinal Detachment.” Invest Ophthalmol Vis Sci. 2000;41:3576–3581
- Hammes HP, Du X . “Benfotiamine blocks three major pathways of hyperglycemic damage and prevents experimental diabetic retinopathy.” Nat Med. 2003 Mar;9(3):294-9. Epub 2003 Feb 18.
- Hipkiss AR, Brownson . “Reaction of carnosine with aged proteins: another protective process?” Ann N Y Acad Sci. 2002 Apr;959:285-94.
- Zachary A. Knight, K. Schot Hannan, Matthew L. Greenberg, Jeffrey M. Friedman. “Hyperleptinemia Is Required for the Development of Leptin Resistance.” PLoS ONE 5(6): e11376. doi:10.1371/journal.pone.0011376.
- Min-Diane Li. “Leptin and Beyond: An Odyssey to the Central Control of Body Weight.” The Yale Journal of Biology and Medicine. 2011;84(1):1-7.
- Eri Suganami, Hitoshi Takagi,Hirokazu Ohashi, Kiyoshi Suzuma, Izumi Suzuma, Hideyasu Oh, Daisuke Watanabe, Tomonari Ojimi, Takayoshi Suganami, Yasushi Fujio, Kazuwa Nakao, Yoshihiro Ogawa and Nagahisa Yoshimura. “Leptin Stimulates Ischemia-Induced Retinal Neovascularization: Possible Role of Vascular Endothelial Growth Factor Expressed in Retinal Endothelial Cells.” Diabetes. September, 2004. vol. 53 no. 9 2443-2448
- Joseph R. Vasselli, Philip J. Scarpace, Ruth B. S. Harris, and William A. Banks. “Dietary Components in the Development of Leptin Resistance.” Adv. Nutr. 2013: 4: 164–175.
- Joseph R. Vasselli. “Fructose-induced leptin resistance: discovery of an unsuspected form of the phenomenon and its significance.” Am J Physiol Regul Integr Comp Physiol. 2008 Nov;295(5):R1365-9. doi: 10.1152/ajpregu.90674.2008. Epub 2008 Sep 10.
- Waltner-Law ME, Wang XL Epigallocatechin gallate, a constituent of green tea, represses hepatic glucose production. J Biol Chem. 2002 Sep 20;277(38):34933-40. Epub 2002 Jul 12.
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
Outside of the Box
Whenever you find yourself on the side of the majority, it is time to pause and reflect.
– Mark Twain
Why should we limit ourselves to thinking outside the box. Can’t we just get rid of the box?
True discovery consists in seeing what everyone has seen . . . then, thinking what no one has thought.
People were burned at the stake because they refused to believe the Earth was not the center of the universe. They were beheaded because they had a sneaking suspicion that the world was not flat.
Is it really that hard to accept that our weight gain and diabetes is driven by a hormonal signal, and not by gluttony or caloric intake of fat?
The challenge with the current thought model on the cause of obesity is that it does not account for metabolic syndrome. In the practice of medicine over the last 15 years, an interesting pattern has emerged. I noticed that there was a spike in fasting and postprandial insulin levels 5-10 years prior to the first abnormal fasting and postprandial blood sugars. These patients were exercising regularly and eating a diet low in fat. But they saw continued weight gain and progressed down the path of metabolic syndrome. 10-15 years later, they fall into the classification of type II diabetes.
The only thing that seems to halt this process in these patients is carbohydrate restriction. Fasting insulin levels return to normal, weight falls off, and the diseases of civilizations disappear as insidiously as they arose.
So you tell me, is the world flat? Is the Earth the center of the universe?
Why Your Oatmeal is Killing Your Libido
Have you noticed that there are a large number of advertisements in the media about checking your testosterone or “Low T” Syndrome? It seems like this is the new advertising trend on the radio and late night TV.
Suddenly, everyone’s testosterone is low and men are complaining about their libido, . . . or are they?
If you practice medicine long enough, you’ll see a trend that seems to have arisen as our waistlines have expanded. About half of the men in my office with insulin resistance, pre-diabetes or diabetes have low testosterone levels. But this shouldn’t be a surprise. Type II diabetes, metabolic syndrome and insulin resistance are all driven by an over production in insulin in response to a carbohydrate load in the meal. Patients with these conditions produce between two to ten times the normal insulin in response to a starchy meal. A number of studies both in animal and human models demonstrate that insulin has a direct correlation on testosterone suppression in the blood. This has been demonstrated in both men and women. In fact, glucose intake has been shown to suppress testosterone and LH in healthy men by suppressing the gonadal hormone axis and more predominant testosterone suppression is seen in patient with insulin resistance or metabolic syndrome.
In fact, to put it simply, insulin increases the conversion (aromitization) of testosterone to estrogen in men (it does the opposite in women). Interestingly, Leptin resistance has a similar effect. I tend to see the worst lowering of testosterone in men with both insulin and leptin resistance.
How to you improve your testosterone? Supplemental testosterone has been shown to help, but it comes with some risks, including prostate enlargement and stimulating growth of prostate cancer. The most natural way to improve your testosterone is to change your diet.
A low carbohydrate or ketogenic diet turns down the insulin production and allows the testosterone to be available for use by the body. A ketogenic diet has the effect of reducing leptin resistance as well through weight loss. A simple dietary change of this type is frequently seen in my office to increase testosterone by 100-150 points.
What is a ketogenic diet? It is a diet that restricts carbohydrates to less than 50 grams per day, thereby causing the body to use ketones as the primary fuel source. So, for breakfast tomorrow morning, hold the oatmeal (1/2 cup of Quaker Instant Oatmeal is 31 grams of carbohydrates) and have the bacon and eggs. And, rather than have the cheesecake for desert this evening, have an extra slice of steak butter on your rib-eye and hold the potato.
Cured . . . by Definition.
A friend posted this image and I couldn’t help but think about this little cartoon throughout the day. In the 15 years that I have been in medical practice, it was re-emphasized to me that my definition of cure and the patient’s definition of cure may at times be notably different or even in opposition.
I am reminded of a sweet a patient in her early nineties that was brought in by her three well meaning and very caring daughters. This patient was a type II diabetic and, for the most part, her blood sugar was in pretty good control. To put it in medical terms, her morning blood sugars were in the 120 range and her Hemoglobin A1c (HbA1c) was a 6.4%. She was obese by the standards of her body mass index (BMI) and her cholesterol was elevated.
The concern of her three daughters, “there to rat her out,” as the patient put it, was that she was eating donuts for breakfast each morning for the last few months. I noted that her HbA1c had gone up from 5.9% at the last visit. We discussed the fact that the change in her dietary intake appeared to have caused the rise in her blood sugar and her cholesterol.
With my affirmation of the cause as ammunition, the patient’s daughters began to individually take shots at her choice of meals over the last year. They did it, I could see because they loved and cared for heir mother. But I noticed the patient’s demeanor change suddenly, and a bit of trust between me and my patient began to slip.
This sweet centenarian turned and looked at me, square in the eye, and then proceeded to give me an education.
“Dr. Nally, do you know how old I am?” she asked.
“Why, yes, you are 93 years old,” I replied.
“And do you know how much longer I am going to be alive on this earth?” she inquired.
“Well, no. I do not know how much longer you will be alive, but I can tell you that you have out lived most of your peers and the average age of most Americans.”
“Then, why the hell are you, and my daughters, worried about me eating a damn do-nut?” she yelled. “My blood sugar is still pretty good and I figure that if I have to be around on this earth any longer, then by stars, I am going to enjoy my favorite breakfast. If it kills me, then so be it. I am going to enjoy it.”
Well, that was that. The cure was to enjoy her last few years upon this earth.
She did just that.
Inflammation Killer – A Ketogenic Diet
A recent study published in the Annals of Internal Medicine demonstrate significant improvement in overall inflammation in type II diabetic patients following a carbohydrate restricted diet versus a low fat calorie restricted diet. Another bit of proof demonstrating what I’ve been seeing in my office over the last 8 years. The study reveals significant improvement in glycemic (blood sugar) control in those following a low carbohydrate diet as well as significant lowering of C-reactive protein, IL-1 and IL-6 over those following a low fat diet. You can see the study here.
Ketogenic Diet Reduces Diabetic Nephropathy
A common problem that arises in patients with diabetes is that of kidney disease or “nephropathy.” Nephropathy is defined as damage to or disease of the filtering system of the kidney. In diabetic patients,
they commonly begin to loose the ability to adequately filter and retain microscopic protein needed in the body. As the blood sugar and insulin levels progressively rise over time, damage to the delicate filtering system of the kidneys occur.
Very impressive results revealing improved kidney function were found in both Type I and Type II diabetic mice placed on a low carbohydrate, or ketogenic, diet in just and 8 week period of time. The nephropathy (reduced passage of protein through the kidneys) was completely reversed in all the mice. This is the first in what I suspect will be a series of articles showing that ketogenic diets have significant effect on reversal of age related and diabetic tissue damage. See the article here.