I hear this all the time. “I can’t eat keto because. . . ”
What is your excuse?
I am amazed at how tightly people cling to these excuses. They are just that excuses. In the 16 years I’ve been training people how to use these diets to treat disease, I have yet to find one that is not just an excuse that covers up the real reason . . .
Check out my video on this:
Is following your Total Cholesterol and LDL-C really that important?
You may be quite surprised.
Watch as we discuss the important markers of heart disease and vascular disease risk. We will talk about how these markers can help you understand what your body is doing in the process of making or reversing atherosclerosis (plaque in the vessels). And, should you really be taking that STATIN (cholesterol lowering) drug? Get the scoop here as Dr. Nally very simply points out how the right diet can and will lower your cholesterol without the use of medications.
Research in the last 10 years points to the small-dense LDL particle as the atherogenic component of cholesterol (Hoogeveen RC et al., Arterioscler Thoromb Vasc Biol, 2014 May; Ivanova EA et al., Oxidative Med Cell Longevity, 2017 Apr). Studies in the last five years have identified that elevated small-dense LDL cholesterol correlates much more closely with risk for inflammation, heart disease and vascular disease (Williams PT, et al. Atherosclerosis. 2014 April; 233(2): 713-720.)
Recent research in the last three years demonstrates that small dense LDL cholesterol is a better marker for prediction of cardiovascular disease than total LDL-C (Hoogeveen RC et al., Arterioscler Thromb Vasc Biol. May 2014, 34(5): 1069-1077l; Ivanova EA et al., Oxidative Med Cell Longev. 2017).
Additionally, higher LDL-C is actually predictive of longer life and has been demonstrated to correlate with longevity (Ravnskov U et al., BMJ Open, 2016 Jun 12;6(6): e010401). And, a low LDL-C actually increases risk of early mortality (Schwartz I et al., Lancet 2001, 358: 351-55).
It is commonly understood that LDL-C will rise with increased saturated fat intake on a ketogenic diet. This has been know and reported in the scientific literature for over twenty years. This is to be expected, because LDL-C is really a measurement of three different LDL sub-particles (“big fluffy, medium, and small dense”). Increased saturated fat intake, while at the same time lowering carbohydrate intake, actually causes a shift in these low density particles to a bigger “fluffier” particle conformation (Griffin BA et al., Clin Sci (Lond), 1999 Sep).
The 2015 British Medical Journal, referenced above, analyzed the relevant 19 peer reviewed medical articles that included over 68,000 participants. This review showed that there is no association of high LDL-C with mortality (meaning that an elevated LDL-C does not lead to an increased risk of death from heart or vascular disease). I realize that, in stark opposition to the landmark review above, The American Heart Association’s Presidential Advisory published their position in the June 20, 2017 issue of Circulation. They stated that saturated fat is the cause of increased LDL-C and they further extrapolated that elevated LDL-C is associated with an increase in death by cardiovascular disease. This boldfaced claim is only based on one single small four year (2009-2013) literature review completed by the World Health Organization with a total of only 2353 participants, most of these studies only lasting 3-5 weeks (not nearly long enough to see fully effective cholesterol changes) and none of which had any focus on carbohydrate intake, insulin levels or LDL sub-particle measurement (Mensink RP, Geneva: WHO Library Cataloguing-in-Publication Data, 2016).
Based upon the most current scientific evidence above and my clinical experience, the large body of evidence above demonstrates the use of total cholesterol and LDL-C to determine vascular disease risk to be ineffective tools. A low carbohydrate/ketogenic diet lowers small dense LDL cholesterol, triglycerides and blood sugar and in many cases, the use of cholesterol drug (STATIN) therapy is not needed and ineffective in comparison with a ketogenic/carbohydrate restricted lifestyle.
Over fifty years of data have demonstrated that creating energy deficit through the reduction in caloric intake is effective in reducing weight. . . However, it is only for the short term (1, 2). The biggest challenge physicians face in the treatment of obesity is that calorie restriction fails when it comes to long-term weight loss.
With the craze and popularity of intermittent fasting, some have claimed that intermittent fasting is more effective in weight reduction. Recent results demonstrate that this may also be incorrect. In the short term evaluation of caloric restriction and intermittent fasting, reduction in 15-20 lbs of weight is effectively seen and the highly publicized Biggest Loser’s losing ~ 120 lbs. Intermittent fasting and alternate day fasting have been shown to be more effective in lowering insulin levels and other inflammatory markers in the short term.
There is, however, controversy over maintaining weight loss beyond 12 months in the calorie restriction, intermittent and alternate day fasting groups. Forty different studies in a recent literature review, thirty-one of those studies looking at forms of intermittent fasting, demonstrate that the majority of people regain the weight within the first 12 months of attempting to maintain weight loss(3, 5). This is, also, what I have seen for over 18 years of medical practice.
Numerous “experts” claim that the only way to reduce fat is “caloric deficit.” Variations through the use of intermittent, long-term or alternate day fasts can be found all over the internet. In regards to calorie restriction, these “experts” with nothing more than a personal experience and a blog to back their claims preach this louder than the “televangelists” preach religion. Based on the faith that many place in this dogma, it could be a religion. What causes belief in this dogma is that weight and fat loss actually does occur with caloric restriction to a point. The average person will lose 20-25 lbs, however, within 12 months of achieving this goal, most people regain all the weight. (No one ever mentions the almost universal problem with long-term weight loss, especially those “experts.”)
Prolonged calorie restricted fasts, intermittent fasts, and alternate day fasts are often grouped together into the fasting approach, causing significant confusion among those that I speak to and counsel in my office. There is great data that alternate day fasts do not have the reduction in resting energy expenditure that prolonged fasting, intermittent fasting and calorie restriction cause. However, none of these approaches appears to solve the problem of weight re-gain after long-term (12-24 months into maintenance) weight loss (3). And, a recent study of 100 men participating in alternate day fasting showed that there was a 38% dropout rate, implying that without close supervision and direction, maintenance of this lifestyle is not feasible for over 1/3rd of those attempting it.
Failure on calorie restricted diets, low fat diets, and intermittent fasting diets with weight regain at twelve to twenty-four months is the most common reason people end up in my office in tears. They’ve fasted, starved themselves, calorie restricted, tried every form of exercise, and still regained the weight. Trainers, coaches and “experts” have belittled them for “cheating” or just not keeping to the diet. Yet, we know that calorie restriction and intermittent fasting cause a rebound in leptin, amilyn, peptid YY, cholecystikinin, insulin, ghrelin, gastric inhibitory peptide and pancreatic poly peptide by twelve months causing ineffective long-term weight loss (6). The dramatic rise in these hormones stimulates tremendous hunger, especially from ghrelin and leptin.
Although less problematic in alternate day fasting, these calorie restricted approaches also cause dramatic slowing of the metabolism at the twelve month mark. In many cases, the metabolic rate never actually returns to baseline, creating even more difficulty in losing further weight or even maintaining weight (6).
Gastric bypass and the gastric sleeve procedures have been touted as the solution to this problem, as they decrease ghrelin, however, 5-10 years later, these patients are also back in my office. They find that 5-10 years after these procedures the weight returns, cholesterol and blood pressure rise, and diabetes returns. These hormones kick into high gear, stimulating hunger in the face of a slowed metabolism, that to date, has been the driver for weight regain in the majority of people. People find it nearly impossible to overcome the hunger. You may have experienced this, I know I have.
So, what is the answer? It’s the hormones. (WARNING – You’ll hear that when your wife is pregnant, too, gentlemen). We are hormonal beings, both in weight gain, and in pregnancy. Trying to preach calorie control to a hormonal being is like showing up at the brothel to baptize the staff. You might get them into the water, but you’re probably not getting them returning weekly to church or pay a tithe.
So, how do you manipulate the hormones in a way to control the rebounding hunger and suppression of metabolism? This is where we put a bit of twist on the knowledge we’ve gained from alternate day fasting. Recent research shows that “mild” energy deficit in a pulsatile manner, that has the ability to mimicking the body’s normal bio-rhythm’s is dramatically effective in reducing weight and maintaining normal hormonal function without cause of rebound metabolic slowing (4).
What does this mean in layman’s terms? It means that if we provide a diet that maintains satiety hormones while providing a period of baseline total energy expenditure needs and a period of mildly reduce caloric intake in a pulsed or cyclic manner, greater weight loss occurs and there is no rebound of weight 1-2 years later.
The main reason I’ve not jumped on the intermittent fasting band wagon is the shift in leptin, amylin, ghrelin and GLP-1 signaling that regularly occurs at the 6-12 month mark. The rebound of these hormones causes weight re-gain and is what prevents successful long-term weight loss. A number of people come to my office and tell me they couldn’t follow a ketogenic diet, so they’re doing intermittent fasting and it works . . . for a while. Then, they end up in my office having hit a plateau or fallen off the wagon and regained all the weight. They are completely confused and don’t understand what happned. Most of them are convinced it’s their thyroid or cortisol and they’ve seen every naturopath and functional medicine doctor in town.
What people really need is a simple approach to long-term weight loss without having to spend the night in the physiology lab every two weeks sleeping under a ventilated hood system.
In my office, once we calculate the basic protein needs daily, we start with a 1:1 ratio of protein to fat. Then, the fat is adjusted up or down based on hunger. Remember, hunger occurs, because your body produces hormones. The addition of fat to a diet that is not stimulating large amounts of insulin resets the hormone patterns back to normal without causing weight gain.
“Sure, Dr. Nally, but what about those people who don’t know if they are hungry, bored, stressed or just have a bacon fixation? You can’t just give them all the fat they want?!”
Why not? Implying that people aren’t smart enough to know when they are full is a bit of a fascist philosophy, don’t you think?
Do people over eat? Sure they do. But, I’ve found that when you give people an antidote to hunger (using fat intake in the presence of stabilized insulin levels) over a few months, people begin to recognize true hunger from other forms of cravings. This is especially true when they keep a diet journal. This gives people the ability to begin listening to their own bodies, responding accordingly and governing their stress, eating, exercise and activity. Keeping a diet journal is key to long-term weight loss. And, isn’t helping people use their own agency to improve their health really what we’re trying to do?
Interestingly, doing this over the years seems to line up with the findings of this year’s MATADOR study in the International Journal of Obesity. They found that mild intermittent energy restriction of about 30-33% for two weeks, then interrupting this with two weeks of a diet that was energy balanced for needs improved both short and long-term weight loss efficiency (4). In looking at my, and my patient’s diet journals, this energy restriction of about 1/3 of needed calories cyclically seems to happens naturally with a ketogenic lifestyle, without even counting calories. (Calories are a swear-word in my office).
What does the correct long-term wight loss program look like in a diet or meal plan? Well, you’ll have to join the Ketogenic Lifestyle 101 Course to see what that really means to you individually. I look forward to seeing you there.
Want to find out more about the Ketogenic Lifestyle 101 course? CLICK HERE.
Have you read my book The Keto Cure? Get a signed copy from me by clicking HERE.
Watch this weekend’s Periscope conversation about why weight loss is slow and why anything that is worthwhile takes time.
You can watch the Periscope Video below:
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).
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:
Today’s Periscope was an exciting one. Do you really need a pre- or post-workout shake or meal? How much protein do you need? What’s the difference between ketosis and ketoacidosis? Is Dr. Nally a ketogenic cheerleader? Get your answers to these and many more questions asked by some wonderful viewers this evening on today’s PeriScope.
https://katch.me/embed/v/5def6bce-4f67-363a-b5f9-3bbec8a8aea2?sync=1
Be sure to check out Dr. Nally’s new podcast called “KetoTalk with Jimmy and the Doc” with the veteran podcaster Jimmy Moore on KetoTalk.com. The first podcast will be available on December 31, 2015. KetoTalk with Jimmy and the Doc will be available for download for free on iTunes.
Stay tuned . . . !
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:
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:
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)
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:
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:
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 . . .
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:
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:
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:
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 . . .
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:
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:
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:
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.
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!!!
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:
“So, Doc, which vitamin should I take?”
I’ve heard this question at least 5-6 times per day for the last 20 years. The problem has been, there hasn’t been just one or two products that fit my or my patient’s needs. I’ve seen many that are close, but no one seems to understand the needed nutrients for insulin resistance, leptin resistance and the tremendous effect adequate nutrients has on inflammation, atherosclerosis, uric acid, sodium balance, cholesterol and blood pressure. That is, until I found a company that would let me design my own vitamin.
Working with a world renowned lab, I put together what I know to be the best ketogenic multivitamin on the market. I give you the “KetoNutritionals Multivitamin.”
It provides the nutrients that we recognize are essential to the TCA (tricarboxylic acid) or Krebs cycle. I call it the Multivitamin Adult Formula, because it has the potential to enhance the body’s ability to use insulin, leptin and regulate normal blood sugar and maintain ketosis. Now, it is essential that I inform you that these statements have not been evaluated by the FDA and that this product is not intended to diagnose, treat, cure, or prevent any disease.
However, 60-65% of pre-diabetic and diabetic patients I see in the office do not correctly convert Folic Acid (Vitamin B9). It is suspected that over 40% of the population in general has a genetic deficiency in the gene that codes for MTHFR. MTHFR (also called methylenetetrahydrofolate reductase) is a genetic sequence that encodes for an essential enzyme in your body that helps make the active form of folate. Your body cannot make folate on its own, so it requires enzymes including the one encoded by the MTHFR gene, to make it from the foods that you eat. MTHFR enzyme also has an important role in making amino acids, the building blocks of proteins, by helping convert the chemical homocysteine to methionine in concert with Vitamin B12. Homocysteine is a harmful chemical made by your body that can damage the lipid membrane of cells leading to damage of the walls of your blood vessels, and may affect your blood clotting. In contrast, methionine is an amino acid required by your body for normal functioning. Supplementing the methylated folate helps to provide the needed components for methionine production. KetoNutritional Multivitamin contains both forms of active isomer, naturally occurring folates. MTHFR deficiency can easily be tested for through a simple saliva test in the office.
The conversion of methionine to SAMe is essential in this pathway. SAMe (pronounced Sammy) is necessary for methylation. It is essential in the formation of neurotransmitters like serotonin and liver detoxification through the methylation pathway. Serotonin is key in the treatment and prevention of depression, chronic pain, and liver detoxification. In a number of cases, just fixing this methylation has dramatically improved symptoms of depression that would have otherwise been treated with strong psychogenic medications.
Cysteine is used by the body as a source of sulfur for detoxification and the production of glutathione. Glutathione is your body’s chief anti-oxidant and protector against all kinds of damage. This is where Vitamin B6 plays a major role. Vitamin B6 is also a cofactor in hundreds of different chemical reactions necessary for healthy hormones like estrogen, and progesterone. It is also essential for the production of neurotransmitters like serotonin, dopamine, and GABA for proper brain function.
KetoEssentials contains the essential vitamins to allow these metabolic pathways to function properly. May people on a ketogenic diet don’t get the full effect of weight loss until adequate Vitamin B12 and Vitamin B6 are supplemented. It also contains Vitamin B1, and carnosine that have been found to decrease the effect of inflammatory glycation and damage caused by higher blood sugars like diabetic retinopathy. High gamma Vitamin E has also demonstrated retinopathy protection.
Alpha lipoic acid combined with biotin has been shown to augment a more natural, healthy insulin secretion thereby promoting a more effective glucose metabolism. Taurine, epigallocatechin gallate (EGCg) from green tea and Vitamin D have all been shown to improve the effect of the insulin you produce.
Improving insulin use and production has a direct effect your triglycerides. We now know that when your triglycerides are “out -of-whack,” leptin transport across the blood brain barrier is affected and this worsens your risk leptin resistance. Leptin is that amazing hormone that tells your brain that your fat cells are “full” and to stop eating.
Vitamin A as a carotenoid acts helps aid immune function and Molybdenum aids in detoxification processes in the body.
Added zinc, taurine and EGCg to reduce the damaging effects that fructose can have in the liver, and also enhancing your insulin signaling. Added zinc also helps stabilize your testosterone and sex hormones.
But, these vitamins and anti-oxidants don’t help if they’re not absorbed correctly, so magnesium, chromium, zinc, manganese and vanadium help to enhance absorption. Correct supplementation of these nutrients may have the effect of normalizing glucose, insulin and leptin levels an reduction in risk for long term cardiovascular disease, diabetic complications, water retention, and more effective weight loss.
#180 Capsule Bottle
TO BUY YOUR BOTTLE
References:
Moat SJ, Doshi SN, Lang D, McDowell IFW, Lewis MJ, Goodfellow J. “Treatment of coronary heart disease with folic acid: is there a future?” American Journal of Physiology – Heart and Circulatory Physiology Published 1 July 2004 Vol. 287 no. 1, H1-H7 DOI: 10.1152/ajpheart.00952.2003
Hipkiss AR, Brownson . Reaction of carnosine with aged proteins: another protective process? Ann N Y Acad Sci. 2002 Apr;959:285-94.
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.
Jacob S, Ruus P, Hermann R, Oral administration of RAC-alpha-lipoic acid modulates insulin sensitivity in patients with type-2 diabetes mellitus: a placebo-controlled trial. Free Radic Biol Med. 1999 Aug;27(3-4):309-14.
Boucher BJ . Inadequate vitamin D status: does it contribute to the disorders comprising syndrome ‘X’? Br J Nutr. 1998 Apr;79(4):315-27.
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.
Maassen JA, Mitochondrial diabetes, diabetes and the thiamine-responsive megaloblastic anaemia syndrome and MODY-2. Diseases with common pathophysiology? Panminerva Med. 2002 Dec;44(4):295-300.
Banks WA, Coon AB, Robinson SM, Moinuddin A, Schultz JM, Nakaoke R, Morley JE. Triglycerides Induce Leptin Resistance at the Blood-Brain Barrier. Diabetes May 2004 vol. 53 no. 5 1253-1260.
