I’ve had many of my patients and followers on social media ask about my continued use of the hashtag #JustKeepEsterifying. Well, here is the answer. Check out the short 4 minute video below to get the answer:
Category: Insulin Resistance
Long-Term Weight Loss: Why So Many Fail
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.
Isn’t Fasting Effective in 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.
Is Calorie Restriction the Only Way to Lose Fat?
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.
Long-Term Weight Loss Failure Brings Tears
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).
Is Gastric Bypass or Gastric Sleeve the Solution?
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.
It’s the Hormones, Baby!
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).
Pulsed Mild Energy Restriction
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.
The Ketogenic Lifestyle is a Pulsed Energy Lifestyle
- First, it is essential to turn off the insulin load. Insulin is the master hormone. This is done by a ketogenic lifestyle that restricts carbohydrates.
- Second, providing adequate protein to supply maintenance of muscle and testosterone is key.
- Third, providing adequate fat is the simple way to maintain leptin, ghrelin, amylin, GLP-1 (among the others) and long-term weight loss. Can you eat too much fat? Of course you can. But, because each of us have differing levels of stress and activity each day, this fat intake becomes the lever for hunger control.
- Fourth, the use of exogenous ketones ensures easily accessible ketone (short chain fatty acids) to modulate adipose (white fat) signaling of the liver without large caloric intake through the portal vein by first pass of liver metabolism. The ketones also help stabilize the gut bacteria. The combination of hormone balance between the liver and fat cells and improvement of gut bacteria suppresses key hunger hormones and aids glucose regulation between the fatty tissues and the liver. Ketones, both endogenous and exogenous, suppress production of TNF-alpha, IL-6, resistin, and stabilize production of adiponectin and leptin from the adipose cells (7, 8, 9).
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.
Give Obese People Fat Ad Libitum?
“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.
References:
- Bronson FH, Marsteller FA. “Effect of short-term food deprivation on reproduction in female mice.” Biol Reprod. Oct 1985; 33(3): 660-7. https://www.ncbi.nlm.nih.gov/pubmed/4052528?dopt=Abstract&holding=npg
- Connors JM, DeVito WJ, Hedge GA. “Effects of food deprivation on the feedback regulation of the hypothalamic-pituitary-thyroid axis of the rat.” Endocrinology. Sep 1985. 117(3): 900-6. https://www.ncbi.nlm.nih.gov/pubmed/3926471?dopt=Abstract&holding=npg
- Seimon RV, Roekenes JA, Zibellini J, Zhu B, Gibson AA, Hills AP, Wood RE, King NA, Byrne NM, Sainsbury A. “Do intermittent diets provide physiological beneftis over continuous diets for weight loss? A systematic review of clinical trials.” Mol Cell Endo. 15 Dec 2015. 418(2): 153-172. https://www.sciencedirect.com/science/article/pii/S0303720715300800
- Byrne NM, Sainsbury A, King NA, Hills AP, Wood RE. “Intermittent energy restriction improves weight loss efficiency in obese men: the MATADOR study.” Int J Obes. 2018. 42:129-138. https://www.nature.com/articles/ijo2017206
- Trepanowski JF, Kroeger CM, Barnosky A. “Effect of Alternate-Day Fasting on Weight Loss, Weight Maintenance, and Cardioprotection Among Metabolically Healthy Obese Adults.” JAMA Intern Med. Jul 2017. 177(7): 930-938. https://jamanetwork.com/journals/jamainternalmedicine/article-abstract/2623528?redirect=true
- Sumithran P, Prendergast LA, Delbridge E, Purcell K, Shulkes A, Kriketos A, Proietto J. “Long-term persistence of hormonal adaptations to weight loss.” N Engl J Med. 27 Oct 2011. 365: 1597-1604. http://www.nejm.org/doi/full/10.1056/NEJMoa1105816
- Asrih M et al., “Ketogenic diet impairs FGF21 signaling and promotes differential inflammatory responses in the liver and white adipose tissue.” PlosOne. 14 May 2015. Open Access. https://doi.org/10.1371/journal.pone.0126364
- Veniant MM et al. “FGF21 promotes metabolic homeostasis via white adipose and leptin in mice.” PlosOne. Jul 2012. Open access. https://doi.org/10.1371/journal.pone.0040164
- Whittle AJ, “FGF21 conducts a metabolic orchestra and fat is a key player.” Endocrinology. 1 May 2016. 157(5): 1722-1724.
What If Salt Actually Improves Blood Pressure & Blood Sugar?
What if increasing your salt intake actually improved your diabetic blood sugar?
What if increasing salt intake actually lowered your blood pressure? Could it be that easy?
Just about every patient that I see has significant worry about salt intake. Some greater than others. In fact, some people are so salt phobic that when I encouraged its use, they called me a “quack” and left my practice. But does salt restriction really work, or is it doing more damage than we think?
That was the question that was asked by Dr. Ames in the American Journal of Hypertension 17 years ago. However, his answer never got a mention. In fact, I’ve been in practice for almost 18 years, and incidentally stumbled upon this article when it was mentioned by a colleague of mine. Granted, it is a small sample of people, only 21 in the study. However, the results are profound.
21 patients with hypertension were randomized to periods of no salt (placebo) and periods of 2 grams (2000 mg) of sodium chloride four times a day (a total of 8 grams of salt per day). Glucose tolerance tests were completed with insulin levels at the end of each intervention period.
Insulin Resistance and Hypertension Improve by Adding Salt
What was noteworthy was that those with insulin resistance and diabetes had improvement in their glucose levels while on sodium supplementation. Those with hypertension had improvement in their blood pressure while on the sodium supplementation. Lastly, those with insulin resistance had a lowering of their insulin levels during the period of increased sodium intake. These findings fly in the face of the dogma that’s been drilled into our heads that “salt is bad!”
“But, you can’t base your findings on a small group of 21 people,” the experts say.
Yes, it is a small study group. However, these findings are what I, also, have seen clinically in my practice for over 13 years.
We know that the average human needs 3 grams of sodium per day and 3 grams of potassium per day. If you’re eating the standard American diet (SAD diet) including processed foods, you’re getting 2-3 grams per day of sodium. In fact, the CDC claims the worst meals for you are:
- Bread
- Processed chicken dinners
- Pizza
- Pasta
However, if your following a low-carbohydrate or ketogenic lifestyle, you won’t be eating the meals above and you’re probably not getting near enough salt. This is the cause of the keto-flu I wrote about a few weeks ago. And, according to the study above, it is a potential driver of our persisting insulin resistance, diabetes and hypertension.
How Much Salt Should I Use?
In my office, I encourage use of 3-4 grams of sodium and 3-4 grams of potassium daily when using a ketogenic lifestyle. That’s approximately 1 1/2 – 2 teaspoons of salt per day. I like Redmond’s RealSalt or if you can’t find it, Himalayan Pink Salt, because the pink sea salts contain sodium, potassium, magnesium and zinc.
Could it be that salt restrictions are making our insulin resistance and blood pressure worse? That’s what the clinical evidences are pointing toward. However, more research is still needed.
Want to know more about a ketogenic life-style? Click the link on KetoLife above to get some basics. If you’re already following a ketogenic lifestyle, then let me help you navigate the bumps and turns by going to the Supplement section above and checking out the products I recommend to jump-start ketosis DocMuscles style!
Until then, I’ll have another piece of bacon, please . . . and, oh, pass the salt!
Why Be In Ketosis? Part IX – Memory
Ketosis plays a major role in lowering blood glucose, insulin and notably improving memory in those with Mild Cognitive Impairment and risk for Alzheimer’s Disease (1). Watch this short 5 minute segment on how a ketogenic lifestyle helps. You can learn about a Ketogenic Lifestyle by reading my blog post: A Principle Based Ketogenic Lifestyle. And you can ramp up your blood ketones in less than 30 minutes by getting exogenous ketones at DynamicKetones.com.
Enjoy!!
References:
- Krikoria R et al. “Dietary ketosis enhances memory in mild cognitive impairment.” Neurobiology of Aging. Feb 2012, Vol 33:2 p 419-425.
Ketogenic Lifestyle Rule #1: There should ALWAYS be bacon in the fridge
I thought that over the next few weeks I’d address a number of Ketogenic Lifestyle Rules that I have adopted. These seem to help and bring a little clarity to one following a Ketogenic Lifestyle or someone on the road to becoming a true “Ketonian.”
The first of these rules is that there should ALWAYS be bacon in the fridge!
We address this rule and some interesting facts around having bacon in the fridge in this evening’s Persicope below. We also address the benefits of journaling, how to help stop binge eating, what are your real protein needs, and red-meat fear-mongering. We even discuss whether or not pigs like bacon. Enjoy!
Links referenced in this video:
Red & Processed Meats: Bacon Fear-Mongering
Calculating Your Protein Needs from Ideal Body Weight
(Just a note: I love Katch.me’s service; however, due to the contract language allowing Katch.me to have unlimited rights to my Periscope Videos, I have withdrawn from Katch and my videos are no longer available on this medium until the contract usage can be modified.)
Is Your Sweetener Making you FAT?
I am frequently asked about the sweeteners that can be used with a low carbohydrate diet. There are a number of sweeteners available that are used in “LowCarb” pre-processed foods like shakes or bars, or in cooking as alternatives to sugar; however, many of them raise insulin levels without raising blood sugar and are not appropriate for use with a true low-carbohydrate/ketogenic diet. You can see and print the article I published clarifying which sweeteners you can use and which ones to avoid in the menu bar above “Sour Truth About Sweeteners” and you can watch last night’s periscope below:
Enjoy!!
PeriScope: Weight Loss, Gut Health & Pond Scum…In The New Year
Good morning from Arizona. I’ve had a few people ask about how gut health relates to a ketogenic diet. This is a great question and one that I think can be answered best by taking a closer look at my natural koi pond and learning a little about pond scum.
So, sit back and look at the similaries between your gut and how nature balances a pond system: Katch.me
Or you can watch the video below:
The four tenets of health that we touch on above that are essential to understand before you can understand gut health:
- The body is a unit and works as such with all parts enhancing the whole
- The body is capable of self-regulation, self-healing, and health-maintenance
- Structure & function are reciprocally interrelated
- Rational treatment of the body must be based upon understanding the principles above and assisting or augmenting those principles
Keys to gut health and pond balancing that we touch on:
- Remove the toxins from entering the system like:
- Antibiotic overuse
- Caffeine
- Artificial Fat
- Artificial Sweeteners
- Repair the system and it’s ability to balance the system
- Takes time
- Provide structure for the bacteria to which it can bind
- Provide essential vitamins and minerals like KetoEnhance & Omega-3 fatty acids
- Periodic Fasting
- Restore the bacteria or flora of the system
- Prebiotics (fermented foods like sauerkraut, kimchi, Japanese natto, etc.)
- Probiotics like Dietary KetoBalance (can be purchased in the office)
- Replace the salts and pH balance where necessary
- Replace electrolytes
- Limit things that shift the pH balance
Hope this gives you a starting point for your New Year!!
Definition of Insanity: Cutting Calories/Restricting Fat & Expecting Weight Loss
Have you been cutting your calories and reducing fat and exercising your brains out and still not seeing the needle on the scale move that much? Persistently and repetitively performing an action that doesn’t produce the desired result is insanity. Cutting calories and reducing fat while expecting weight loss is akin to pouring water in the gas tank of your car and expecting it to run smoothly. Why do we do it? Are the 53, 000, 000 people with health club and gym memberships this year really insane?
This evening on PeriScope we touch on fat phobic insanity and the limiting step that actually turns weight gain on or off. (We knew about this in the 1960’s, we just ignored it.)
You can see tonight’s PeriScope with the rolling chat-box questions here at Katch.me/docmuscles. Or, you can watch the video stream below:
The only way to successfully loose weight is to modify or turn off the mechanisms that stimulate fat storage. For years we have been told that this was just a problem of thermodynamics, meaning the more calories you eat, the more calories you store. The solution was, thereby, eat less calories or exercise more, or both. We are taught in school that a 1 gram of carbohydrate contains 4 kcal, 1 gram of protein contains 4 kcal, and 1 gram of fat contains 9 kcal.
If you ascribe to the dogma that weight gain or loss is due to thermodynamics, then it’s easy to see that cutting out fat (the largest calorie containing macro-nutrient) would be the best way limit calories. For the last 65 years, we as a society have been doing just that, cutting out fat, exercising more (with the idea of burning off more calories) and eating fewer calories.
What has this dogma done for us? It’s actually made us fatter! (1)
Some may argue that we really aren’t eating fewer calories and exercising more. But most people I have seen in my office have tried and tried and tried and failed and failed and failed to loose weight with this methodology. In fact, the majority of my patients attempt caloric restriction, exercise and dieting multiple times each year with no success. The definition of insanity is “doing the same thing over and over and expecting a different result.”
Most of my patients are not insane, they recognize this and stop exercising and stop restricting calories . . . ’cause they realized, like I have, that it just doesn’t work!
If you’re one that is still preaching caloric restriction and cutting out fat, I refer you to the figure above and the definition of insanity . . . your straight-jacket is in the mail.
So, if reducing the calories in our diet and exercising more is not the mechanism for turning on and off the storage of fat, then what is?
Before I can explain this, it is very important that you appreciate the difference between triglycerides and free fatty acids. These are the two forms of fat found in the human body, but they have dramatically different functions. They are tied to how fat is oxidized and stored, and how carbohydrates are regulated.
Fat stored in the adipose cells (fat cells) as well as the fat that is found in our food is found in the form of triglycerides. Each triglyceride molecule is made of a “glyceride” (glycerol backbone) and three fatty acids (hence the “tri”) that look like tails. Some of the fat in our adipose cells come from the food we eat, but interestingly, the rest comes from carbohydrates
(“What! Fat comes from sugar?! How can this be?!!“)
We all know that glucose derived from sugar is taken up by the cells from the blood stream and used for fuel, however, when too much glucose is in the blood stream or the blood sugar increases above the body’s comfort zone (60-100 ng/dl), the body stores the excess. The process is called de novo lipogenesis, occurring in the liver and in the fat cells themselves, fancy Latin words for “new fat.” It occurs with up to 30% (possibly more if you just came from Krispy Kream) of the of the carbohydrates that we eat with each meal. De novo lipogenesis speeds up as we increased the carbohydrate in our meal and slows down as we decrease the carbohydrate in our meal. We’ve known this for over 50 years, since it was published by Dr. Werthemier in the 1965 edition of the Handbook of Physiology (2).
While we know that fat from our diet and fat from our food is stored as triglyceride, it has to enter and exit the fat cell in the form of fatty acids. They are called “free fatty acids” when they aren’t stuck together in a triglyceride. In their unbound state, they can be burned as fuel for the body within the cells. I like to think of the free fatty acids as the body’s “diesel fuel” and of glucose as the body’s version of “unleaded fuel.” The free fatty acids can easily slip in and out of the fat cell, but within the adipose cell, they are locked up as triglycerides and are too big to pass through the cell membranes. Lipolysis is essentially unlocking the glycerol from the free fatty acids and allowing the free fatty acids to pass out of the fat cell. Triglycerides in the blood stream must also be broken down into fatty acids before they can be taken up into the fat cells. The reconstitution of the fatty acids with glycerol is called esterification. Interestingly, the process of lipolysis and esterification is going on continuously, and a ceaseless stream of free fatty acids are flowing in and out of the fat cells. However, the flow of fatty acids in and out of the fat cells depends upon the level of glucose and insulin available. As glucose is burned for fuel (oxidized) in the liver or the fat cell, it produces glycerol phosphate. Glycerol phosphate provides the molecule necessary to bind the glycerol back to the free fatty acids. As carbohydrates are being used as fuel, it stimulates increased triglyceride formation both in the fat cell and in the liver, and the insulin produced by the pancreas stimulates the lipoprotein lipase molecule to increased uptake of the fatty acids into the fat cells (3).
So when carbohydrates increase in the diet, the flow of fat into the fat cell increases, and when carbohydrates are limited in the diet, the flow of fat out of the fat cells increases.
Summarizing the control mechanism for fat entering the fat cell:
- The Triglyceride/Fatty Acid cycle is controlled by the amount of glucose present in the fat cells (conversion to glycerol phosphate) and the amount of insulin in the blood stream regulating the flow of fatty acid into the fat cell
- Glucose/Fatty Acid cycle or “Randle Cycle” regulates the blood sugar at a healthy level. If the blood glucose goes down, free fatty acids increase in the blood stream, insulin decreases, and glycogen is converted to glucose in the muscle and liver.
These two mechanisms ensure that there is always unleaded (glucose) or diesel fuel (free fatty acids) available for every one of the cells in the body. This provides the flexibility to use glucose in times of plenty, like summer time, and free fatty acids in times of famine or winter when external sources of glucose are unavailable.
The regulation of fat storage, then, is hormonal, not thermodynamic. Unfortunately, we’ve know this for over 65 years and ignored it.
We’ve ignored it for political reasons, but that’s for another blog post . . .
References:
1. James, W. J Intern Med, 2008, 263(4): 336-352
2. Wertheimer, E. “Introduction: A Perspective.” Handbook of Physiology. Renold & Cahill. 1965.
3. Taubs, G. “The Carbohydrate Hypothesis, II” Good Calorie, Bad Calorie. Random House, Inc. 2007, p 376-403.
Why the Calorie is NOT King
Today in the office I had the calorie conversation again . . . three times. We have an entire society with a very influential health and fitness industry built around the almighty calorie. Has it helped? Looking at our 5 year obesity outcomes. It hasn’t helped a bit. In fact, it is worse. In 1985 only 19% of U.S. adults were obese.
In 2014, 34.5% of U.S. adults were obese. The numbers this year are approaching 35.6% You can see the dramatic increase in obesity by 1-3% every year for the last 5 years in the CDC images above.
For over 50 years we have been told that caloric restriction and fat restriction is the solution. But by the numbers above, the 58 million people in the U.S. utilize a gym or health club to burn off those calories aren’t seeing the success that they should be expecting.
Why? Because the calorie is NOT king. What do I mean by that? We don’t gain weight because of the thermogenic dogma we’ve been taught for the last 50 years. Our weight gain is driven by a hormone response to food. Hear more about why the calorie is NOT king on tonight’s PeriScope. You can Katch it here with all the live stream comments and hearts at Katch.me/docmuscles.
Or you can watch the video without the comments here:
Pre-, Post-Workout Meal on Ketosis. Is it Important?
Today’s Periscope was an exciting one. Do you really need a pre- or post-workout shake or meal? How much protein do you need? What’s the difference between ketosis and ketoacidosis? Is Dr. Nally a ketogenic cheerleader? Get your answers to these and many more questions asked by some wonderful viewers this evening on today’s PeriScope.
https://katch.me/embed/v/5def6bce-4f67-363a-b5f9-3bbec8a8aea2?sync=1
Be sure to check out Dr. Nally’s new podcast called “KetoTalk with Jimmy and the Doc” with the veteran podcaster Jimmy Moore on KetoTalk.com. The first podcast will be available on December 31, 2015. KetoTalk with Jimmy and the Doc will be available for download for free on iTunes.
Stay tuned . . . !
The 3 Weight Loss Necessities to Weathering the Holidays
What are the three things you need to successfully weather the holidays with your ketosis lifestyle? What does a raindeer on a motorcycle look like? How does insulin resistance effect kidney stones and gout? How do you get back on track if you fall off the ketosis wagon? These and many more questions are answered by Dr. Adam Nally on tonight’s PeriScope.
You can see the video stream including the comment roll here at katch.me/docmuscles. Or you can watch the video below:
How Do You Know if You’re Insulin Resistant?
How do you know if you're insulin resistant? What questions need to be asked? What should your numbers be? And, many other great ketosis questions. Also, why does Dr. Nally look like he has dirt on his chin? See it here . . .
Common Ketosis Killers
“I’ve tried your low-carb diet, Dr. Nally, and it didn’t work.”
“Hmm . . . really?” If you’re mumbling this to yourself, or you’ve said it to me in my office, then lets have a little talk. You’ve probably been subjected to the common ketosis killers.
I’ve heard this statement before. It’s not a new statement, but it’s a statement that tells me we need to address a number of items. If you’ve failed a low carbohydrate diet, I’d suspect you are pretty severely insulin resistant or hyperinsulinemic. You probably never really reached true ketosis. I’d want to have you checked out by your doctor to rule out underlying disease like hypothyroidism, diabetes, other hormone imbalance, etc.
Nutritional Ketosis is Most Effective as a Lifestyle Change
Next, switching to a low-carbohydrate lifestyle is literally a “lifestyle change.” It requires that you understand a few basic ketosis principles. And, it takes the average person 3-6 months to really wrap their head around what this lifestyle means . . . and, some people, up to a year before they are really comfortable with how to eat and function in any situation.
I assume, if you are reading this article, that you’ve already read about ketosis and understand the science behind it. If not, please start your reading with my article The Principle Based Ketogenic Lifestyle – Part I and Ketogenic Principles – Part II. If this is the case, then please proceed forward, “full steam ahead!”
There are usually a few areas that are inadvertently inhibiting your body transformation, so let’s get a little personal.
Nutritional Ketosis is a Very Low Carbohydrate Diet
First, this is a low carbohydrate diet. For weight loss, I usually ask people to lower their carbohydrate intake to less than 2o grams per day. How do you do that? (A copy of my diet is accessible through my membership site HERE.) You’ve got to begin by restricting all carbohydrates to less than 20 grams per day. Any more than 20 to 30 grams per day will cause an insulin release from the pancreas and stimulate fat storage of both carbohydrate and fat for the next 10-12 hours, commonly killing ketosis. Keep a dietary journal to record your progress, your cravings, your successes and failures. I’m going to want to see it and review it with you if you see me.
No, I don’t believe in “Net Carbs.” Net Carbs are a sales gimmick to get you to buy “artificial food” that keeps you coming back for “artificial food” and halts your weight loss (you’ll see why shortly). You’re going to lose the most weight and feel your best when you eat real food. I do allow for the subtraction of real fiber, specifically non-cooked, non-blended, non-juiced leafy greens (If you cook, blend or juice a leafy green, it activates more carbohydrate availability). Leafy greens are real fiber. You can subtract them. In fact, I recommend eating 1-3 cups of leafy greens per day to help bowel function & provide necessary folic acid, but, everything else is “carbage.” Avoid it.
Yes, cottage cheese and yogurt contain carbohydrates. Be very cautious with them.
No, oatmeal and Cream of Wheat™ are not helpful. See my article on Why Your Oatmeal is Killing Your Libedo.
Alcohol also halts your weight loss. It’s not the sugar in the alcohol I’m worried about, the distilling process changes the sugar to alcohol, however, alcohol stimulates an insulin response after the alcohol is metabolized in the liver with a SIMILAR RESPONSE to regular sugar.
To Effectively Maintain Nutritional Ketosis, You MUST get adequate Protein
Second, this is a low carbohydrate, moderate protein, high fat lifestyle. N0 . . . it is NOT a high protein diet! However, so many of my patients don’t eat enough protein that they feel like it is a “high protein diet.”
Protein is essential for the building and maintaining of muscle, connective tissue and a number of other enzymatic reactions in your body. However, in patients who are morbidly obese [people with a body mass index (BMI) over 50], excess protein intake can cause fat to be stored by producing an excessive insulin response. In these patients we initially moderate protein. Excess sugars and a number of proteins, in the presence of a high insulin response, are converted to triglyceride (the soft squishy stuff inside the fat cells that make them plump) and stocked away inside your adipose tissue. Excessive protein, especially the amino acids argenine, leucine and tryptophan are common ketosis killers, not because they are converted to sugar, but because they stimulate and insulin response all by themselves.
If you don’t fall into the morbidly obese category (BMI over 50). Then, I encourage you to use the protein levels below.
Initially, I ask my patients to focus on lowering their carbohydrate intake and I don’t really worry about protein. (It is often hard enough to figure out what the difference between a carbohydrate and a protein in the first month or two if you’ve never had any nutrition background.) Most people begin losing weight just by lowering carbohydrates over the first few months. Once you figure out how to lower your carbohydrates, if your weight loss is not moving and your pants are not getting looser, then you’re probably eating too much protein.
How much protein do you need? It’s pretty easy to calculate and is based on your height and gender. Your basic protein needs to maintain muscle, skin and hair growth are as follows:
- 70 grams or higher for women per day
- 120 grams or higher for men per day.
However, these levels are WAY TOO LOW for weight loss and maintaining good health. Because we now know that protein acts as a hormone in a number of ways, in my office I recommend women get 80-90 grams of protein per day, and men should get > 150 grams of protein per day.
If you’re still a little confused about protein, read my article on Why Your Chicken Salad Stops Your Weight Loss.
This also goes for protein powders and protein shakes. Many of these have 25-40 grams of protein in them per serving, so be careful with their use.
Nutritional Ketosis is a High Fat Diet
Third, this is a high fat lifestyle. Yes, I want you to INCREASE your fat intake. I’m going to repeat that, again, just for clarity, . . . . INCREASE your fat intake. Increase it to around 50% of your total calories, . . . 70% of your total calories if you can do it. Not enough fat is a common ketosis killer.
“What?! Won’t that cause heart disease and stroke and make my cholesterol worse?!!!”
I know, take a big deep breath . . . (you may even need to breath into a paper bag for a minute if you begin hyperventilating).
No, it will not raise your cholesterol, cause heart disease, or cause a stroke. If you have lowered your carbohydrate intake to less than 20 grams per day, then there is NO hormonal signal for you to make more bad cholesterol, worsen heart disease, or cause a stroke. In fact, there is great data showing that increasing your fat and lowering your carbohydrates reverses the blockage in the arteries. I see this reversal every single day in my clinic through the application of ketogenic diets.
If we remove carbohydrate as your primary fuel, you must replace it with something else.That something else should be fat. Protein must be moderated, as it will also be stored as fat if you eat too much. So, if the carbohydrates are kept low, fat intake can be increased and the body will pick the fat it wants and essentially throw the rest out without raising cholesterol, causing weight gain or causing heart disease. This is why we want you to use good natural animal fats like butter, hard cheese, olive oil, coconut oil, avocado, etc. Look for fats highest in omega-3 fatty acids as these decrease inflammation and improved weight loss. Look for meats highest in fat like red meat (55% fat) and pork (45% fat). Take the food pyramid and flip it over.
Check Your Sweeteners At the Door
The fourth common ketosis killer and culprit in halting your weight loss is artificial sweeteners. There are quite a few of them. Most of them WILL cause an insulin response (exactly what we don’t want for weight loss) with minimal to no rise in blood sugar. Raising blood sugar doesn’t matter, if the insulin is being stimulated . . . “you’re gonna gain weight for the next 10-12 hours.” I wrote an article for you to print off and hang on your fridge, upload it to your iPhone or carry it with you in your purse to the grocery store. (If you’re a man and you’re carrying a purse, please don’t tell me about it.) You can find the article here: The Skinny About Sweeteners. The short list of those sweeteners that are OK to use and cook with, and do not increase insulin response, can be found here in my Amazon Store.
Don’t Even Start with Coffee Creamers
Fifth on my list is coffee creamer. Coffee creamer contains corn syrup solids (another very special name for . . . SUGAR!!) and/or maltodextrin (SUGAR’s married name!). If you must put something in your coffee, then use real heavy cream (pure tasty fat) or real butter. It will taste much better (I’m told – I don’t drink coffee personally) and you won’t get an insulin spike 2-3 hours later and begin craving more coffee and donuts.
Yes, “Half & Half” is half fat and half sugar. . . avoid it too!!
Ketosis Killing Medications
The sixth culprit in halting weight loss is medications. Please talk to your doctor before making ANY changes in your medications as suddently stopping them can be hazardous to your health. Those highest on my list for stopping your weight loss are Glyburide (glipizide), insulin, & steroids like prednisone. A more complete list of medications that will halt your weight loss can be found on my on my ketogenic diet plan. If you are on any prescription medications, please talk to your doctor or to a physician board certified in obesity medicine treatment about how to adjust or wean these medications in a way that is safe and appropriate for your individual needs.
Estrogen
The seventh common culprit in halting weight loss is a lack of estrogen in menopausal or post-menopausal women. About 20% of women that I see in my practice who are over 55 years old, need some degree of estrogen replacement before they are able to lose weight. Estrogen plays a very large role in regulation of the metabolism and when deficient, causes weight retention or weight gain. Talk to your doctor about the risks and benefits of estrogen for you individually in this situation.
Stress
The eighth reason for shifting out of ketosis is stress. Acute and chronic stress can be caused by a number of issues. The most common is lack of sleep. You can read about stress and ways to address it in two of my articles: How Does Stress Cause Weight Gain? and Adrenal Insufficiency, Adrenal Fatigue and PseudoCushing’s Syndrome – Oh My!
For many years, we’ve thought that caffeine was great for weight loss. However, we are finding, clinically, that too much caffeine can also cause a stress response by raising cortisol, releasing glycogen, thereby stimulating an insulin response and bringing your weight loss to a screeching halt. How much caffeine? . . . The jury is still out . . . and remains to be determined. But, I am currently under going an n=1 experiment on myself (as many of you know, I loved Diet Dr. Pepper. But I had to give it up). I’ll keep you posted . . .
Look closely at these eight issues. Correcting them usually solves most plateaus with weight loss and improves blood pressure, blood sugar and cholesterol control dramatically.
Adrenal Insufficiency, Adrenal Fatigue, PseudoCushing’s Syndrome – Oh My!
Adrenal Fatigue? Adrenal Insufficiency? Cortisol? PseudoCushing’s Syndrome? What do these terms mean and why are they all over the internet these days? And, what do they have to do with your weight loss?
This was our topic this evening on PeriScope. Katch Dr. Nally speak about this topic with rolling comments at Katch.me/docmuscles. Or you can watch the video below:
If you’re not sure about what this is, you’re not alone. I think I’ve heard the term “Adrenal Fatigue” at lease four times a day for the last three months. If you ask your doctor, they’ll probably scratch their heads too. The funny thing is that “Adrenal Fatigue” isn’t a real diagnosis, but it is all over the internet and it shows up in the titles of magazines in the grocery store every day. There’s even and “Adrenal Fatigue For Dummies” so it must be real, right?!
No. It isn’t a real diagnosis. It is a conglomeration of symptoms including fatigue, difficulty getting out of bed in the morning, and “brain fog” that have been lumped together to sell an “adrenal supplement.” (Sorry, but that’s really what it is all about.) Do a Google search and the first five or six sites describing adrenal fatigue claim the solution is taking their “special adrenal supplement.”
I know what you’re thinking, “Your just a main stream, Western Medicine doctor, Dr. Nally, you wouldn’t understand.” Actually, I do understand.
Adrenal fatigue has risen in popularity as a “lay diagnosis” because many patients show up at their doctors office with significant symptoms that actually interfere with their ability to function, and after all the testing comes back negative for any significant illness, they are told that they are normal. But the patient still has the symptoms and no answer or treatment has been offered. It’s discouraging. . . very discouraging.
That’s because the symptoms are actually the body’s response to chronic long term stress. Many of my patients, myself included, have found themselves “stuck” in their weight loss progression, feeling fatigued, struggling to face the day, with a number of symptoms including cold intolerance, memory decline, difficulty concentrating, depression, anxiety, dry skin, hair loss, and even infertility in some cases. Is it poor functioning adrenal glands? No, your feeling this way because the adrenal glands are actually doing their job!!
If the adrenal glands weren’t working you’d experience darkening of the skin, weight loss, gastric distress, significant weakness, anorexia, low blood pressure, and low blood sugar. The symptoms are actually called Addison’s disease and it is actually fairly rare (1 in 100,000 chance to be exact). So what is causing the symptoms you ask?
There are a number of reasons, but one that I am seeing more and more frequently is “Pseudo-Cushings’s Syndrome.” Pseudo-Cushing’s Syndrome is a physiologic hypercortisolism (over production of cortisol) that can be caused by five common issues:
- Chronic Physical Stress
- Severe Bacterial or Fungal Infections that Go Untreated
- Malnutrition or Intense Chronic Exercise
- Psychological Stress – including untreated or under-treated depression, anxiety, post-traumatic stress, or dysthymia (chronic melancholy)
- Alcoholism
The psychiatric literature suggest that up to 80% of people with depressive disorders have increased cortisol secretion (1,2,3). People with significant stressors in their life have been show to have an increased corsiol secretion. Chronic stress induces hyperactivity of the hypothalamic-pituitary-adrenal axis causing a daily, cyclic over production of cortisol and then normalization of cortisol after resolution of the stressor. This cortisol response is not high enough to lead to a true Cushing’s Syndrome, but has the effect of the symptoms listed above and begins with limiting ones ability to loose weight.
I’m convinced that this is becoming more and more prevalent due to the high paced, high-stress, always on, plugged in, 24 hour information overload lives we live.
What is cortisol? It is a steroid hormone made naturally in the body by the adrenal cortex (outer portion of the adrenal gland). Cortisol is normally stimulated by a number of daily activities including fasting, awakening from sleep, exercise, and normal stresses upon the body. Cortisol release into the blood stream is highest in the morning, helping to wake us up, and tapers into the afternoon. Cortisol plays a very important role in helping our bodies to regulate the correct type (carbohydrate, fat, or protein) and amount of fuel to meet the bodies physiologic demands that are placed upon it at a given time (4,5,6).
Under a stress response, cortisol turns on gluconeogensis in the liver (the conversion of amino acids or proteins into glucose) for fuel. Cortisol, also, shifts the storage of fats into the deeper abdominal tissues (by stimulating insulin production) and turns on the maturation process of adipocytes (it makes your fat cells age – nothing like having old fat cells, right?!) In the process, cortisol suppresses the immune system through an inhibitory effect designed to decrease inflammation during times of stress (7,8,9). If this was only occurring once in a while, this cascade of hormones acts as an important process. However, when cortisol production is chronically turned up, it leads to abnormal deposition of fat (weight gain), increased risk of infection, impotence, abnormal blood sugars, brain fog, head
aches, hypertension, depression, anxiety, hair loss, dry skin and ankle edema, to name a few.
The chronic elevation in cortisol directly stimulates increased insulin formation by increasing the production of glucose in the body, and cortisol actually blunts or block-aids the thyroid function axis. Both of these actions halt the ability to loose weight, and drive weight gain.
Cortisol also increases appetite (10). That’s why many people get significant food cravings when they are under stress (“stress eaters”). Cortisol also indirectly affects the other neuro-hormones of the brain including CRH (corticotrophin releasing hormone), leptin, and neuropeptide Y (NPY). High levels of NPY and CRH and reduced levels of leptin have also been shown to stimulate appetite and cause weight gain (10-11).
How do you test for Pseudo-Cushing’s Syndrome?
Testing can be done by your doctor with a simple morning blood test for cortisol. If your cortisol is found to be elevated, it needs to be repeated with an additional 24 hour urine cortisol measurement to confirm the diagnosis. If Cushing’s Syndrome is suspected, some additional blood testing and diagnostic imaging will be necessary. Pseudo-Cushing syndrome will demonstrate a slightly elevated morning cortisol that doesn’t meet the criteria for true Cushing’s type syndrome or disease.
How do you treat it?
First, the stressor must be identified and removed. Are you getting enough sleep? Is there an underlying infection? Is there untreated anxiety or depression present? Are you over-exercising? These things must be addressed.
Second, underlying depression or anxiety can be treated with counseling, a variety of weight neutral anti-depressant medications or a combination of both. Many of my patients find that meditation, prayer, and journaling are tremendous helps to overcoming much of the anxiety and depression they experience.
Third, adequate sleep is essential. Remove the television, computer, cell phone, iPad or other electronic distraction from the bedroom. Go to bed at the same time and get up at the same time each day. Give yourself time each day away from being plugged in, logged in or on-line.
Fourth, mild intensity (40% of your maximal exertion level) exercise 2-3 days a week was found to lower cortisol; however, moderate intensity (60% of your maximal exertion level) to high intensity (80% of your maximal exertion level) exercise was found to raise it (12). A simple 20 minute walk, 2-3 times per week is very effective. Find a hobby that you enjoy and participate in it once or twice a week. Preferably, a hobby that requires some physical activity. The activity will actually help the sleep wake cycles to improve.
Fifth, follow a low carbohydrate or ketogenic diet. Ketogenic diets decrease insulin and reverse the effect of long term cortisol production. Ketogenic diets a have also been shown to decrease or mitigate inflammation by reducing hyperinsulinemia commonly present in these patients (13).
So, the take home message is . . . take your adrenal glands off of overdrive.
References:
- Pfohl B, Sherman B, Schlechte J, Winokur G. Differences in plasma ACTH and cortisol between depressed patients and normal controls. Biol Psychiatry 1985; 20:1055.
- Pfohl B, Sherman B, Schlechte J, Stone R. Pituitary-adrenal axis rhythm disturbances in psychiatric depression. Arch Gen Psychiatry 1985; 42:897.
- Gold PW, Loriaux DL, Roy A, et al. Responses to corticotropin-releasing hormone in the hypercortisolism of depression and Cushing’s disease. Pathophysiologic and diagnostic implications. N Engl J Med 1986; 314:1329.
- Ely, D.L. Organization of cardiovascular and neurohumoral responses to stress: implications for health and disease. Annals of the New York Academy of Sciences (Reprinted from Stress) 771:594-608, 1995.
- McEwen, B.S. The brain as a target of endocrine hormones. In Neuroendocrinology. Krieger and Hughs, Eds.: 33-42. Sinauer Association, Inc., Massachusetts, 1980.
- Vicennati, V., L. Ceroni, L. Gagliardi, et al. Response of the hypothalamic- pituitary-adrenocortical axis to high-protein/fat and high carbohydrate meals in women with different obesity phenotypes. The Journal of Clinical Endocrinology and Metabolism 87(8) 3984-3988, 2002.
- Wallerius, S., R. Rosmond, T. Ljung, et al. Rise in morning saliva cortisol is associated with abdominal obesity in men: a preliminary report. Journal of Endocrinology Investigation 26: 616-619, 2003.
- Epel, E.S., B. McEwen, T. Seeman, et al. Stress and body shape: stress-induced cortisol secretion is consistently greater among women with central fat.
Psychosomatic Medicine 62:623-632, 2000. - Tomlinson, J.W. & P.M. Stewart. The functional consequences of 11_- hydroxysteroid dehydrogenase expression in adipose tissue. Hormone and Metabolism Research 34: 746-751, 2002.
- Epel, E., R. Lapidus, B. McEwen, et al. Stress may add bite to appetite in women: a laboratory study of stress-induced cortisol and eating behavior.Psychoneuroendocrinology 26: 37-49, 2001.
- Cavagnini, F., M. Croci, P. Putignano, et al. Glucocorticoids and neuroendocrine function. International Journal of Obesity 24: S77-S79, 2000.
- Hill EE, Zack E, Battaglini C, Viru M, Vuru A, Hackney AC. Exercise and circulating cortisol levels: the intensity threshold effect. J Endocrinol Invest. 2008. Jul;31(7):587-91.
- Fishel MA et al., Hyperinsulinemia Provokes Synchronous Increases in Central Inflammation and β-Amyloid in Normal Adults. Arch Neurol. 2005;62(10):1539-1544. doi:10.1001/archneur.62.10.noc50112.
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 . . .
Diabetes Mellitus – Really the Fourth Stage of Insulin Resistance
I just completed my reading of Dr. Joseph Kraft’s Diabetes Epidemic & You. This text originally printed in 2008 and was re-published in 2011. I am not really sure why I have never seen this book until now, but I could not put it down. I know, I am a real life medical geek. But seriously, you should only read this book if you are concerned about your health in the future. Otherwise, don’t read it.
For the first time in 15 years, someone has published and validated what I have been seeing clinically in my office throughout my career. Dr. Kraft is a pathologist that began measuring both glucose and insulin levels through a three hour glucose tolerance blood test at the University of Illinois, St. Joseph Hospital in Chicago. This test consists of checking blood sugar and insulin in a fasted state, and then drinking a 100 gram glucose load followed by checking blood sugar and insulin at the 30, 60, 120 and 180 minute marks (a total of three hours).
Dr. Kraft completed and recorded this test over a period of almost 30 years on 14,384 patients between 1972 and 1998. His findings are landmark and both confirm and clarify the results that I have seen and suspected for years.
I am convinced that our problem with treating obesity, diabetes and the diseases of civilization has been that we defined diabetes as a “disease” based on a lab value and a threshold instead of identifying the underlying disease process. We have been treating the symptoms of the late stage of a disease that started 15 to 20 years before it is ever actually diagnosed. Diabetes is defined as two fasting BS >126, any random blood sugar >200, or a HbA1c >6.5%. (Interestingly this “disease” has been a moving target. When I graduated from medical school it was two fasting blood sugars >140 and the test called hemoglobin A1c (HbA1c) that we use today for diagnosis didn’t even exist). The semantics associated with this problem is that many of us recognize that the disease is not actually diabetes. The disease is (as far as we understand it today) insulin resistance or hyperinsulinemia. This is where Dr. Kraft’s data is so useful. Diabetes, as it is defined above, is really the fourth stage of insulin resistance progression over a 15-20 year period and Dr. Kraft’s data presents enormous and very clear evidence to that effect.
When I first entered private practice 15 years ago, I noticed a correlation and a very scary trend that patients would present with symptoms including elevated triglycerides, elevated fasting blood sugar, neuropathy, microalbuminuria, gout, kidney stones, polycystic ovarian disease, coronary artery disease and hypertension that were frequently associated with diabetes 5-15 years before I ever made the diagnosis of diabetes mellitus. I began doing 2 hour glucose tolerance tests with insulin levels and was shocked to find that 80-85% of those people were actually diabetic or very near diabetic in their numbers. The problem with a 2 hour glucose tolerance test, is that if you are diabetic or pre-diabetic, you feel miserable due to the very profound insulin spike that occurs. A few patients actually got quite upset with me for ordering the test, both because of how they felt after the test, and the fact that I was the only physician in town ordering it. So, in an attempt to find an easier way, I found that the use of fasting insulin > 5 nU/dl, triglycerides > 100 mg/dl and small dense LDL particle number > 500 correlated quite closely clinically with those patients that had positive glucose tolerance tests in my office. There is absolutely no data in the literature about the use of this triangulation, but I found it to be consistent clinically.
I was ecstatic to see that Dr. Kraft plowed through 30 years and over 14,000 patients with an unpleasant glucose tolerance test and provided the data that many of us have had to clinically triangulate. (I’m a conservative straight white male, but if Dr. Kraft would have been sitting next to me when I finished the book this afternoon, I was so excited that I probably would have kissed him.)
Insulin resistance or hyperinsulinemia (the over production of insulin between 2-10 times the normal amount after eating carbohydrates) is defined as a “syndrome” not a disease. What Dr. Kraft points out so clearly is that huge spikes in insulin occur at 1-2 hours after ingestion of carbohydrates 15-20 years prior to blood sugar levels falling into the “diabetic range.” He also demonstrates, consistently, the pattern that occurs in the normal non-insulin resistant patient and in each stage of insulin resistance progression.
The information extrapolated from Dr. Kraft’s research give the following stages:
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:
- Kraft, JR. Diabetes Epidemic & You: Should Everyone Be Tested? Trafford Publishing, 2008, 2011. p 1-124
- Boyle JP et al. Projection of the year 2050 burden of diabetes in the US adult population: dynamic modeling of incidence, mortality, and prediabetes prevalence, http://www.pophealthmetrics.com/content/8/1/29 Accessed November 22, 2015
How to Stay Motivated on Carbohydrate Restriction
This evening on PeriScope, we talked about the 10 things you can do to stay motivated on your low-carb lifestyle. A number of great questions were asked including:
- How much carbohydrate should be restricted?
- What labs should you be monitoring regularly?
- What’s a normal blood sugar?
- Why is Dr. Nally freezing in Denver?
- Is fermented food good for you?
- Why should you eat pickles and kimchi even when you’re not pregnant?
And, much much more . . . It’s like a college ketogenic course on overdrive . . . for FREE!!!
You can see the PeriScope with the comments rolling in real-time here: katch.me/docmuscles
Or, you can watch the video stream below:
See you next time.
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
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Lily's Chocolate . . . It's Quite Tastey!!
We just got a sample pack of Lily’s Chocolate. This is a Stevia and erythritol sweetened chocolate that has no aftertaste and doesn’t cause the stomach upset that many experience with chicory root based products. I am always looking for good low carbohydrate alternatives for snacks, as rescue foods, or to assist in baking.
My wife found this chocolate in a recipe that Carolyn Ketchum had posted on her website, All Day I Dream About Food. It is quite tastey!! Thanks, Caroyln!! (By the way, I dream about food all day long, too.)
I scanned a copy of the wrapper for the Salted Almond & Milk Flavor. I have to admit, I ate half the bar. It was that good!!
For those looking for an alternative chocolate for a snack or to use in a recipe, this may be the answer. You can find their whole line of chocolates here.
Hope this helps.
Why Does Your Chicken Salad Stop Weight Loss?
I have multiple patients that come to my office that we follow and treat for weight loss and metabolic syndrome. They are discouraged that their weight loss has stopped or is very, very slow. The most frequent problem I find when they bring in their food journals is the “healthy chicken salad.”
“What?! But, Doc, Chicken Salad is healthy?! RIGHT?”
The chicken salad shows up on their journal almost daily. Somehow, we’ve been indoctrinated that the chicken salad is good for us. I want you to look closely at the image that was recently shared on the internet below. How is the nutrient value of your chicken salad any different than the Big Mac?
Why is this unhealthy? The carbohydrate content greater than 20-30 grams will cause a spike in insulin. When insulin spikes, the body is told to store fat (and it will store fat for up to 12 hours) . . . Yes, the 24 grams of fat in the salad now become dangerous in the presence of an insulin spike. In my patients with metabolic syndrome, they will produce between two and ten times the insulin and store two to ten times the fat. (Ten Big Macs would have tasted better . . . )
There is actually more carbohydrate in your salad than in the big mac. Why not add a strawberry shake just to finish putting the nail in the coffin? And we wonder why we are having trouble with weight loss?
The other issue, and probably of even greater importance, is that chicken breast has the second highest content of lysine & argenine (two of the 10 essential amino acids) count of all the poultry family. This is second only to turkey breast, which also contains a large amount of tryptophan (a third essential amino acid that spikes insulin). Why is this a problem? Because argenine, tryptophan and lysine all stimulate an insulin response on their own, separate from glucose. We need these amino acids, however, when our meals contain a predominance of these amino acids, it rasies insulin significantly in those who are insulin resistant (pre-diabetic).
Those 43 carbohydrates, plus the stimulus from a meat high in argenine, lysine and tryptophan, spike your insulin, kick you out of nutritional ketosis and slow weight loss for up to 48 hours.
Please, if you are following a low-carb or ketogenic diet, get rid of the chicken salad.
If you want to learn more about this, read my article on the eight most common reasons you can’t lose weight.