Hair loss is an issue that I am asked about quite frequently. With any dietary change, transient hair loss can occur in the first 2-3 months but will usually resolve. Continued hair loss is a problem with any diet and if you are experiencing hair loss it could be due to one of five issues:
1. Medication
2. Lack of protein or caloric restriction
3. Hypothyroidism
4. Iron Deficiency
5. Hormone imbalance (especially estrogen dominance or poly-cystic ovarian syndrome)
Dr. Nally discusses these and how to address them in his most recent YouTube video. Check it out below.
Our celebration of Independence Day is a deception.
Laying beneath the fireworks, barbecue and fun is the hard to swallow truth . . . It’s all a sham.
Are you and I really independent anymore? No. Not anymore.
243 years ago, the British oppression was a threat. It was singular, visible and involuntary.
Now, the threat we face daily is an entirely new form of tyranny, infinitely more complex.
The scary thing is that oppression is now:
Fractionated
Invisible
Voluntary
Fractionality of Our Millennial Tyranny
Slavery has changed. The oppressor previously owned the slave individually. However, with time we learned that when there are multiple owners, the burden of ownership is lessened. Joint ownership became the norm. Now we have joint ownership of our condos, boats, and jets. The burden of slave ownership was the risk of revolt and revolution.
If ownership of debt can be spread among the masses, the individual risk is mitigated.
Our fractional oppression is spread throughout the legion, and the tyranny is masked as a principle of the great “free market.”
BIG FOOD sells cancer, diabetes, heart disease and fatigue through the FOMO of fake food.
BIG MEDIA sprinkles us with malaise, despair, anxiety and post-traumatic stress with lurid half-truths, click-bait shock value, and salty emotion all with the intent to sell us more advertisement.
BIG PHARMA peddles side-effects, addiction and false hope convincing the feeble mind, created by BIG FOOD, that a pill is necessary to prevent us from experiencing the pain, emotion and struggle of life – that same life that BIG MEDIA keeps ever present in the palms of our hands. In bed with BIG GOVERNMENT, their evangelism recommends medicating instead the more difficult learning from struggle and failure.
BIG GOVERNMENT covers us with red tape to stop the financial bleeding and hemorrhaging of the tumor’s growth it stimulates, through greed and invasion of individual inalienable right.
BIG MONEY circles us on wings of dread and fear singing a song of doom, all the while sampling emotional cookies and Danishes of immediate gratification, while slipping the “plastic card with a security chip” shackles over the wrists of the enslaved.
BIG EDUCATION preys upon our children with glib platitudes, group-think, and participation trophies. It teaches the weakened minds to prize test-taking, rote memorization, and fact regurgitation above problem-solving, creative thinking, and learning from failure. They prepare our children to work as drones on the factory floor of cyberspace instead of art and enterprise.
And, that’s just the beginning.
Look no further than your bank statement to see how the oppression is itemized. Each line item takes it’s pound of flesh round the clock each month.
Invisibility of Oppression
“None are more hopelessly enslaved than those who falsely believe that they are free.” -Goethe-
200 years ago, the shackles were visible.
Today the shackles are disguised. Independence is a deception.
We are smarter than an outright shackle. So, they were re-tooled, re-imagined, re-formed, and hidden like landmines in cyberspace:
0% APR
Matching contributions
Free Miles
Free Samples
No Money Down
84 Month Installments
These are just grease on the slaughterhouse chute.
It Can’t Be Oppression if You & I Now Volunteer?
Forced slavery is no longer acceptable in our “free society.” The dark genius of modern oppression is the creation of cultural norms, rituals and addiction that invite us to PUT ON OUR OWN CHAINS.
Modern slavery is now VOLUNTARY.
“No one put a gun to your head or forced you to buy our product or service,” is the mantra of the oppressor while billions are spent on engineering conditions that make the shackles look like icing on your cyberspace cake.
But there is an escape . . .
Massive in scale, fractional, and nearly invisible, there is still a choice.
CHOICE IS THE ESCAPE
So, this evening, as the cardboard tubes of fireworks lay discarded in the park grass, and the toy flags lay rolled up on top of the fridge, awaiting their return to the attic for storage, let your Independence Day celebration be much deeper. Choose.
Let your Independence Day stir the same indignation for oppression that our fore-fathers felt.
Cultivate within yourself the desire to fight and win a second Independence Day.
You will need every ounce of resolve and strength you can muster.
Today, there are no chains, hangman’s noose or firing squads, there is but chemistry, habit, choice and instinct. The Oppressor will attempt to use it against you. You can still see it if you look. You can still choose.
Have the courage to flip them the bird of indignation as they present you the “standard American prepackaged life.”
Reject What Isn’t Real
Reject the drama and depletion of paycheck-to-paycheck living . . . instead, create wealth. Save a few dollars each day.
Reject the cardboard food in the grocery store and eat real food: bloody, fresh and wild. It will re-energize you.
Reject the FOMO of the dutiful consumer and become a CREATOR. Create the world you dream of by small and simple daily choices.
Reject the fake new, fake government, fake food, fake medicine, fake success, fake friendships, and fake happiness that encircles us. Create a life that is REAL. You’ll know it’s real because you can feel it, beyond the pain of trial and error and failure, REAL encompasses heart, mind, body and soul at the same time.
Take off the blinders so that you may see the leeches and parasites sticking to you. Rip them from your body and warm yourself as you burn them in the fire.
Only then will you escape the clutches of the modern tyrant.
Only then will you be free.
[Adapted from Bryan Ward and his “Third Way Man” series]
Adam S. Nally, D.O. (aka DocMuscles)
If you enjoy my content, please checkout the links below:
What do you do when you hit a weight loss stall while living a ketogenic lifestyle? Find out below. Dr. Nally goes into detail on the multiple causes of stalling while following a low-carbohydrate or ketogenic lifestyle. He dispels the myths around counting calories and macros. And, he discussed the basics of overcoming a stall.
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.
I’ve opened up my ketogenic weight loss class to the public. Come and join us if you are struggling to lose weight. Many people are struggling to understand how a ketogenic diet works, or finding confusion with all of the different “experts” teaching people to live a ketogenic lifestyle.
Come join me this Friday, and lets put you on a course for success.
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.
N Eng J Med 27 Oct 2011. Mean (±SE) Fasting and Postprandial Levels of Ghrelin, Peptide YY, Amylin, and Cholecystokinin (CCK) at Baseline, 10 Weeks, and 62 Weeks.
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).
N Engl J Med 27 Oct 2011. Mean changes is weight from 0 – 62 weeks.
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
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 May2016. 157(5): 1722-1724.
How does ketosis help the diseases of civilization? Find out as Dr. Nally answers these and many other pertinent dietary questions this evening.
You can learn more about his multi-vitamin supplement he designed for insulin resistance/diabetic/weight management patients that he mentions in the video here at KetoLiving.com.
You can learn about exogenous ketones that he mentions helps to augment ketosis here at DymaicKetones.com.
What is Insulin Resistance? Dr. Nally talks about the nuts and bolts of this syndrome and how it works. He answers multiple questions regarding diet and insulin resistance. Let me know what you thing and what questions future videos should answer.
Many people ask me, “Dr. Nally, why should I always be in ketosis even if I burn fat and lose weight without restricting carbohydrates as much as you do?”
The answer is fat burning efficiency. Shifting into ketosis changes your ability to burn fat, and do it efficiently by turning on cGMP in the adipocyte. I explain how below:
Enjoy!! You can click the link below to ramp up your ketosis through the use of exogenous ketones at DynamicKetones.com. Yes, I make a profit from the sale of exogenous ketones, but I just gave you the magic bullet for opening up the adipocyte for FREE!
If you are interested in the low-carb, moderate protein, high-fat, ketogenic diet, then this is the podcast for you. We zero in exclusively on all the questions people have about how being in a state of nutritional ketosis and the effects it has on your health. There are a lot of myths about keto floating around out there and our two amazing cohosts are shooting them down one at a time. Keto Talk is cohosted by 10-year veteran health podcaster and international bestselling author Jimmy Moore from “Livin’ La Vida Low-Carb” and Arizona physican and certified bariatric physician Dr. Adam Nally from “Doc Muscles” who thoroughly share from their wealth of experience on the ketogenic lifestyle each and every Thursday. We love hearing from our fabulous Ketonian listeners with new questions–send an email to Jimmy at livinlowcarbman@charter.net. And if you’re not already subscribed to the podcast on iTunes and listened to the past episodes, then you can do that and leave a review HERE. Listen in today as Jimmy and Adam answer more engaging questions about nutritional ketosis from you the listeners today in Episode 17!
We’ve never really seen a man or an elephant in long term ketosis before . . .
“It’s a snake.”
“It’s a wall.”
“It’s a rope.”
“It’s a fan.”
“It’s a tree.”
“It’s insulin resistance.”
I’ve always been fascinated by those describing a “new finding” in medicine. I am reminded of the story of 5 men who, never having seen an elephant before, were blindfolded and asked to describe what he discovered. However, each man was introduced to a different part of the elephant. Each of them had a dramatically different description of the elephant and each made a conclusion that was very different from the others.
What is fascinating, is that we usually make our “blindfolded comparisons” to those things we have seen or about which we have some descriptive understanding. Observing and describing human physiology is much like examining an elephant while blindfolded for the first time.
This week’s “blind-folded finding” is what has been interpreted by some as “insulin resistance” made worse by a ketogenic diet. Really? This perked my curiosity, because I’ve personally been following a low-carbohydrate/ketogenic diet for years and have thousands of patients doing the same. To this day, I’ve never seen insulin resistance “get worse.” In fact, it gets better. Clinically, it seems to take about 18-24 months to improve, but, it usually gets better.
THE QUESTION –
I’ve had three people from around the world contact me this week and ask why, after being on a ketogenic diet and “in ketosis,” they suddenly get a notably large blood glucose spike when they cheat. By notably large, I mean that their blood sugars rise to over 200 mg/dl within 2 hours of a carbohydrate containing meal. Now, they admit to rapid glucose recovery within an hour or two, and their hemoglobin A1c levels are subjectively normal (less than 5.6%). The worry is “am I becoming diabetic?” They also complain that after having been in ketosis for longer than 3-4 months, they cannot get their fasting blood sugars below 100 mg/dl.
Those asking me the question about this anomalous “physiological insulin resistance” referred to a couple of off-the-cuff blogger’s posts from 2-3 years ago referencing a few small studies (some of which were very poorly designed) [here, here, here & here] in the journals from 10-20 years ago. These articles describe a physiologic response interpreted as worsening “insulin resistance.” However, if you understand what is actually occurring in the Ketonian (yes, I made that term up – there will soon be a whole village of us), I see it as a normal physiologic response. It is misinterpreted by those who’ve never actually seen long term ketogenic physiology, as anomalous, in the average human.
THE ANSWER –
I’ve been seeing this slight elevation in fasting blood sugar with normal or low normal HbA1c in myself and many of my patients for quite some time. However, I never saw it as “insulin resistance” worsening. Clinically, when I tease out the food logs, it usually ends up being protein intake is too high, the person is using a sweetener or creamer causing rebound morning glucose elevation or, in those with low normal HbA1c’s (4.3-5.6%), it is in actuality a protective mechanism of “physiologic glucose sparing” in the keto-adapted individual (1, 2).
It can very easily be explained when one understands how ketones are actually used in the keto-adapted individual. First, a wonderful figure below (Thank you for pointing me to this one, Dr. Peter Attia) found in Dr. Veech et. al.’s paper (3) gives us an overview of how ketones skirt the TCA cycle within the mitochondria of the cell, causing inhibition of pyruvate dehydrogenase leading to glucose sparing by the cells of the brain that still require it’s availability (Oh, by the way, this is how we survived harsh winters and famines).
From the Figure 1 above, you can see that beta-hydroxybuterate [BHB (a ketone)] is converted to acetoacetyl CoA leading to the production of pyruvate, block-aiding additional glycolysis or inhibiting further glucose production at the liver level. Because the muscle tissues become more adept at using BHB, GLUT receptors are down-regulated at the muscle level as a person becomes more keto-adapted. Although we still have much to learn about the keto-adapted state, we know that this occurs more prominently in the muscle tissues than in the gut and brain. This fascinating glucose sparing phenomenon, has been interpreted by some as “worsening insulin resistance.”
Not to worry, glucose sparing is rapidly reversible and transitory within 1-3 days of increasing carbohydrate intake above 100-150 grams per day (1). It is also why those who become keto-adapted get a carbohydrate hangover including headache, stomach cramps, diarrhea, and malaise lasting 8-24 hours after cheating.
Is this bad? Absolutely not! It is NORMAL! (It’s just that most people, physicians included don’t know what the normal physiology of the Ketonian should look like.) Is it going to kill you, cause a stroke or give you a heart attack? Absolutely not. The elevated BHB actually increases production of adiponectin, leucine & glutathione that have antioxidant properties protecting one from transient inflammatory rises in blood sugar, enhancing insulin’s effect on the muscle, and preserving muscle mass while allowing for fat metabolism (4, 5, 6).
THE TAKE-HOME MESSAGE –
First, don’t cheat if you don’t want to see transient rises in blood sugar and experience the wonders of a carbohydrate hangover and some mild reactive hypoglycemia (low blood sugar) after the fact.
Second, if you’ve been in ketosis for longer than 3-4 months, and you absolutely must get another two or three hour oral glucose tolerance test (OGTT), you might want to increase your carbohydrate intake to 50-100 grams per day 1-3 days before the test to avoid an anomalous spike in blood glucose. (One OGTT was enough for me . . . but hey, some of us are gluttons for punishment.)
Third, enjoy your eggs, pass the bacon and stir me up some Keto//OS.
KetoOS – Drinkable Exogenous Ketones
References:
Kinzig KP, Honors MA, Hargrave SL. Insulin sensitivity and glucose tolerance are altered by maintenance on a ketogenic diet. Endocrinology 151: 3105–3114, 2010.
Oliveira Caminhotto R, Lima FB. Impaired glucose tollerance in low-carbohydrate diet: maybe only a physiological state. American Journal of Physiology – Endocrinology and Metabolism Published 15 December 2013 Vol. 305 no. 12, E1521 DOI: 10.1152/ajpendo.00580.2013
Veech RL, Chance B, Kashiwaya Y, Lardy HA, Cahill GF Jr. Ketone bodies, potential therapeutic uses. IUBMB Life. 2001 Apr;51(4):241-7.
The image above has nine dots within a square. Your task, using only four lines is to connect ALL nine dots WITHOUT ever raising your pen, pencil or finger (Please don’t use a sharpie on your computer screen . . . it doesn’t come off).
You may have seen this puzzle previously . . . it’s made its rounds in corporate training circles. But the underlying principle remains true. The solution requires you to expand your thinking or to “think outside the box.”
Whenever you find yourself on the side of the majority, it is time to pause and reflect. (Mark Twain)
Why should we limit ourselves to thinking outside the box. Can’t we just get rid of the box?
True discovery consists in seeing what everyone has seen . . . then, thinking what no one has thought.
The answer can be found when those four lines are used beyond the box our mind creates:
What good has the box done us? People were burned at the stake because they refused to believe the Earth was not the center of the universe. People were beheaded because they had a sneaking suspicion that the world was not flat.
Why is it so very hard to accept that our weight gain and diabetes are driven by a hormonal signal, and not by gluttony or caloric intake of fat? The definition of insanity is doing the same thing repetitively and expecting a different outcome. How long have you been restricting calories and fat with only minimal or no improvement in your weight, blood sugar, cholesterol or general feeling of health?
The main problem with the current thought model, or dogma, on the obesity’s cause is that it does not account for metabolic syndrome. Metabolic syndrome is insulin resistance. It is an over production of insulin in the presence of ANY form of carbohydrate (sugar or starch).
In the practice of medicine over the last 15 years, I noticed that a very interesting pattern emerged. There was always a spike in fasting and postprandial insulin levels 5-10 years prior to the first abnormal fasting and postprandial blood sugars. These patients were exercising regularly and eating a diet low in fat. But they saw continued weight gain and progressed down the path of metabolic syndrome. 10-15 years later, they fall into the classification of type II diabetes. What I now lovingly refer to as stage IV insulin resistance.
The only thing that seems to halt this progressive process with any degree of success is carbohydrate restriction. Fasting insulin levels return to normal, weight falls off, and the diseases of civilizations seem to disappear as insidiously as they arose.
So you tell me, is the world flat? Is the Earth the center of the universe?
What is a low carbohydrate or ketogenic diet? 15 years of practical in the trenches experience have helped me develop a very simple program to help you lose and maintain your weight. Access to this program, video help and access to blog articles at your fingertips are offered through my online membership site.
You can also hear me each week a I discuss low carbohydrate, paleolithic and ketogenic diets with the Legendary Jimmy Moore on KetoTalk.com
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!!
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)
Obesity Rates Around the World
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?!!“)
De Novo Lipogenesis
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.
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.
U.S. Obesity Adult 2011U.S. Adult Obesity 2014
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:
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.
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.
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:
This evening we covered the 5 myths of weight loss identified through the National Weight Control Registry’s research findings. What causes “wrinkle face” for Dr. Nally? We also talked about & answered 20 minutes of rapid fire questions ranging from the amount of protein you need daily to the likelihood a human could be a bomb calorimeter . . . exciting stuff!!
You can watch the video stream below. Or you can Katch the replay with the rapid stream of exciting comments here at Katch.me/docmuscles.
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:
Diseases seem to arrive in three’s each day in my office. Today I had three different patients with cholesterol concerns who were notably confused about what actually makes the cholesterol worse, and what causes weight gain. Each of them, like many patients that I see, were stuck in a state of confusion between low fat and low carbohydrate lifestyle change. My hope is to give my patients and anyone reading this blog a little more clarity regarding what cholesterol is, how it is influenced and how it affect our individual health.
First, the standard cholesterol profile does not give us a true picture of what is occurring at a cellular level. The standard cholesterol panel includes: total cholesterol (all the forms of cholesterol), HDL (the good stuff), LDL-C (the “bad” stuff) and triglycerides. It is important to recognize that the “-C” in these measurements stands for “a calculation” usually completed by the lab, and not an actual measurement. Total cholesterol, HDL-C and triglycerides are usually measured and LDL-C is calculated using the Friedewald equation [LDL = total cholesterol – HDL – (triglycerides/5)]. (No, there won’t be a quiz on this at the end . . . so relax.)
However, an ever increasing body evidence reveals that the concentration and size of the LDL particles correlates much more powerfully to the degree of atherosclerosis progression (arterial blockage) than the calculated LDL concentration or weight (1, 2, 3).
There are three sub-types of LDL that we each need to be aware of: Large “fluffy” LDL particles (type I), medium LDL particles (type II & III), and small dense LDL particles (type IV).
Weight & Size of VLDL, LDL & HDL
Why LDL-C is misleading: Identical LDL-C of 130 mg/dL can have a low risk (Pattern A) with a few “big fluffy LDL particles or high risk (Pattern B) with many small dense LDL particles.
Second, it is important to realize that HDL and LDL types are actually transport molecules for triglyceride – they are essentially buses for the triglycerides (the passengers). HDL can be simplistically thought of as taking triglycerides to the fat cells and LDL can be thought of as taking triglycerides from the fat cells to the muscles and other organs for use as fuel.
Third, it is the small dense LDL particles that are more easily oxidized and because of their size, are more likely to cause damage to the lining of the blood vessel leading to damage and blockage. The large boyant LDL (“big fluffy LDL particles”) contain more Vitamin E and are much less susceptible to oxidation and vascular wall damage.
Eating more fat or cholesterol DOES NOT raise small dense LDL particle number. Eating eggs, bacon and cheese does not raise your cholesterol! What increases small dense LDL particles then? It is the presence of higher levels of insulin. Insulin is increased because of carbohydrate (sugars, starches or fruits) ingestion. It is the bread or the oatmeal you eat with the bacon that is the culprit. The bread or starch stimulates and insulin response. Insulin stimulates the production of triglycerides and “calls out more small buses” to transport the increased triglyceride to the fat cells (4, 5, 6, 7).
Fourth, following a very low carbohydrate diet or ketogenic diet has been demonstrated to decreased small dense LDL particle number and correlates with a regression in vascular blockage (8, 9). So, what does this really mean to you and me? It means that the low-fat diet dogma that that has been touted from the rooftops and plastered across the cover of every magazine and health journal for the last 50 years is wrong. . . absolutely wrong.
I talk about this and answers questions on today’s Periscope. You can see the recording on Katch.me with the comments in real time here:
Superko HR, Gadesam RR. Is it LDL particle size or number that correlates with risk for cardiovascular disease? Curr Atheroscler Rep. 2008 Oct;10(5):377-85. PMID: 18706278
Rizzo M, Berneis K. Low-density lipoprotein size and cardiovascular risk assessment. QJM. 2006 Jan;99(1):1-14. PMID: 16371404
Rizzo M, Berneis K, Corrado E, Novo S. The significance of low-density-lipoproteins size in vascular diseases. Int Angiol. 2006 Mar;25(1):4-9. PMID:16520717
Howard BV, Wylie-Rosett J. Sugar and cardiovascular disease: A statement for healthcare professionals from the Committee on Nutrition of the Council on Nutrition, Physical Activity, and Metabolism of the American Heart Association. Circulation. 2002 Jul 23;106(4):523-7. PMID: 12135957
Elkeles RS. Blood glucose and coronary heart disease. European Heart Journal (2000) 21, 1735–1737 doi:10.1053/euhj.2000.2331
Stanhope KL, Bremer AA, Medici V, et al. Consumption of Fructose and High Fructose Corn Syrup Increase Postprandial Triglycerides, LDL-Cholesterol, and Apolipoprotein-B in Young Men and Women. The Journal of Clinical Endocrinology and Metabolism. 2011;96(10):E1596-E1605.
Shai I et al. Cirulation. 2010; 121:1200-1208
Krauss RM, et al. Prevalence of LDL subclass pattern B as a function of dietary carbohydrate content for each experimental diet before and after weight loss and stabilization with the diets. American Journal of Clinical Nutrition. 2006; 83:1025-1031
Gentile M, Panico S, et al., Clinica Chimica Acta, 2013, Association between small dense LDL and early atherosclerosis in a sample of menopausal women, Department of Clinical Medicine and Surgery, University “Federico II” Medical School, Naples, Italy Division of Cardiology, Moscati Hospital, Aversa, Italy A. Cardarelli Hospital, Naples, Italy
The most exaggerated “frowney” face I get in the office seems to occur when patient’s find out that they cannot eat oatmeal or cereal any longer when following a low-carbohydrate dietary lifestyle. No, oatmeal is NOT good for you . . . I don’t care what WebMD recently said. No, steel-cut oats are even worse (1/4th cup of steel-cut oats is 27 grams of carbohydrate – Who only eats 1/4th cup of oatmeal? Most people eat at least 1/2 -1 cup at a sitting. You do the math . . .)
When I mentioned this to a disabled patient, even her service dog frowned.
Now, before you go running to Larry, the Quaker Oats Mascot (he’s been around for over 140 years), and ask his weight loss advise, I have the solution.
Larry, the Quaker Oats mascot loses 10 lbs for new 2012 cover (He finally figures it out after 137 years)
My angelic wife, Tiffini, the amazing homestead chef and animal husbandry specialist on our little farm, started making low-carb granola for our horseback trail rides. Prior to our discovery of a ketogenic lifestyle, granola was a staple in our pantry, on road trips and in the saddle bags on the trail. This has now replaced any craving either of us had for granola. It carries nicely all day in a Ziplock bag on horseback. It even tastes fantastic in a bowl with unsweetened almond milk as a breakfast alternative if you’re tired of eggs and bacon (but, who ever tires of eggs and bacon? I know . . . Right?!!)
I’ve been nibbling from this actual cookie-sheet of low-carb granola while writing this post. . . I wish you were here to share it with. Soooooo very good, and good for your ketogenic lifestyle. I think I’m going to eat another handful while I finish up Part II of the Principle Based Ketogenic Lifestyle post. Enjoy . . .
In a food processor, process the almonds and 1 cup of the pecans until it resembles coarse crumbs. Using a knife (preferably a sharp one – remember all bleeding stops eventually), chop the remaining 1/4 pecans coarsely.
Melt the butter and place it in mixing bowel or mixer (We use a Kitchen Aid Mixer). Pour the coarsely chopped nuts into the mixing bowl. Stir in flax seed meal, sunflower seeds, coconut flakes, pepitas and vanilla whey protein powder. Blend in the remaining wet mixture, egg whites and add a pinch of salt. Mix until it forms “clumps.”
Spread the mixture evenly on a large wax paper covered baking or cookie sheet and bake at 350 degrees F for 20-25 minutes or until golden brown. Let it cool on the baking sheet to crisp up for a few hours.
It can be stored in a Ziplock bag in the refrigerator.
It has been resoundingly clear to me over the last couple of weeks that there is a tremendous need for a principle based approach to a ketogenic diet. This approach, however, must be simple. So many of the approaches to weight loss I read about are complex and the questions that arise from these approaches are innumerable. Losing weight should not be as difficult as putting a man on the moon. To quote a patient recently, “If it ain’t simple, Doc, I ain’t doing it. . .”
I agree.
Any approach that requires the conversion of food to numbers or calories or exchanges becomes cumbersome, and I personally won’t follow it for more than a week. The principle based approach should be simple and is really based upon the mantra:
Give a man a fish and he will eat today. Teach a man to fish and he will eat for the rest of his life.
Ketogenic diets are wrongly referred to as diets. What I’m talking about is a ketogenic lifestyle. Simple lifestyle design should not be hard. So, what do you say? Shall we learn to fish?!
I assume that if you’re reading this article, you already understand that weight gain is not due to an over intake of calories. Weight gain is due to hormone signals throughout the body leading to the storage of fat . . . specifically, triglycerides being taken up into the fat cells. The hormone that independently controls uptake of fat into each fat cell is insulin. Insulin is an essential hormone, but too much of it stimulates the adipose (fat cells) to over-stock triglycerides or essentially “get fat.” It, actually, is that simple. There’s really only one rule to this lifestyle: If it raises your insulin it will halt or stall your weight loss. Write that on your hand or your forehead or in your planner, the lifestyle revolves around that one rule.
Most people start a ketogenic diet because they want to lose weight and have failed at multiple other dietary approaches. Reasons for weight control failure are often multi-faceted, but they all start with from a position of flawed understanding. The majority of approaches to weight management come from the false assumption that weight is gained because of an over-consumption of calories or a lack of physical activity to burn excess calories. People have faithfully been restricting calories and exercising to exhaustion since the early 1980’s to no avail. (Well, 1% of people succeed, but the rest of us failed this approach). The definition of insanity is repetitive completion of an ineffective action and expecting a different outcome each subsequent time around. If you still think that caloric restriction and exercise is successful, I’ll be shipping your drawstring white vest and your invitation to a padded cell shortly.
Let me put it clearly. We’ve been exercising and cutting our calories since 1975 and look at what it’s gotten us . . .
. . . . a country that is now recognized as the “United States of Corpulence.” Super-Size me has become literal. “Houston . . . we have a problem . . . !”
The rule above is based on foundational principles. Understanding of the principles allows one to successfully apply the rule above.
PRINCIPLE 1
The first principle in a ketogenic lifestyle is understanding that the problem is not caloric, but hormonal. Choices and actions from here on out must be based on this understanding. Anything that will raise insulin will thwart ketosis. Insulin stimulates lipoprotein lipase, the enzyme that pulls the triglycerides into the fat cells. Without insulin, we don’t gain weight. (That’s why type I diabetes are usually very slender and skinny).
The standard lab value for normal fasting insulin levels reflect 10-22 uIU/L as the normal. However, in my office, glucose tolerance tests and postprandial glucose tests consistent with impaired fasting glucose are routinely positive when the fasting insulin level is >5 uIU/L.
Point of Focus: If your having trouble, look at the hormones. Food stimulates hormone responses. Focus on the hormone response to your diet.
PRINCIPLE 2
A ketogenic diet is one where the body uses fatty acids as the primary fuel. Those triglycerides mentioned above are made up of three fatty acids linked to a glycerol molecule. To use the triglycerides, the three fatty acids must be broken away from the glycerol by hormone sensitive lipase (HSL). Insulin directly inhibits HSL. Keeping insulin levels low is the first step in shifting to a ketogenic metabolism. Lowering insulin allows access to the fatty acids in your fat cells. Triglycerides are not water soluble and the rate by which they can be taken up and burned in the mitochondria limits the speed by which triglycerides can be used as fuel. The by product of triglyceride burning is ketones. Ketones themselves can be used as fuel and over 4-6 weeks, the body can enhance its ability to use ketones when fat is the primary fuel. This is called “Keto-Adaptation.”
Point of Focus: Too much carbohydrate in the diet shifts the body from it’s use of fat and triglycerides back to glucose. In general, to become “keto-adapted,” limit carbohydrate to < 20 grams per day. Keep protein at around 0.8 to 1 gram of protein per pound of body weight.
KetoOS – Drinkable Exogenous Ketones
PRINCIPLE 3
Wait a minute!? Where do the ketones come in? When fatty acids are burned or oxidized in the mitochondria of cells within the liver, they are converted into Acetyl-CoA. The Acetyl-CoA is used to form ATP for energy in the Citric Acid Cycle.
IF excess Acetyl-CoA production occurs or if inadequate oxaloacetate is present, the extra Acetyl-CoA is transformed into ketone bodies – specifically beta-hydroxybutyric acid and acetoacetic acid. Fat can be oxidized or burned for fuel while ketones are being produced. Ketones are much smaller molecules and can more easily be transported in the blood than triglycerides, as they are water soluble. The ketones themselves can also be used or burned as fuel as the body upregulates the mitochondria’s ability to use the ketones as fuel as well. As I mentioned above, this process of “keto-adaptation” can take 4-6 weeks. Keto-adaptation results in humans having a greater desire to be physically active – the miraculous conversion of the couch-potato into the bacon-burning triathlete.
Point of Focus: Sugar is a drug. Its byproduct has the same hedonic effect on the brain as morphine. Sugar withdrawal can commonly cause headache, anxiousness, insomnia, dizziness, fatigue and moodiness within the first week of carbohydrate restriction on the road to keto-adaptation.
PRINCIPILE 4
For the average person to become “ketotic” or reach a state of ketosis, it takes lowering the carbohydrates to less than 20 grams per day (and sometimes less than 10 grams per day) for at least 3-7 days. Yes, it can actually take a week to reach ketosis. I have a few patient’s that are so insulin resistant that it takes longer. This means that to reach that fat burning state, one must maintain a low insulin response by restricting starch or carbohydrate intake to less than 20 grams per day for a minimum of a week. For your body to efficiently use the fuel it can take up to 6 weeks. This is why many people state that they “don’t feel good” or “can’t maintain their exercise levels” when starting a ketogenic diet. For most people, once they reach the 6 week mark, mitochondria have been unregulated and “fine tuned” to burn ketones, fat burning becomes efficient and energy levels begin to increase. In fact, for many like myself, you’ll finally feel like exercising for the first time in you life.
Point of Focus: If you’re already exercising, don’t be surprised if you feel more sluggish for the first four weeks. If you’re not exercising, I don’t recommend starting until after you pass through the Keto-Adaptive phase.
PRINCIPLE 5
Clinically, the average patient in my office will lose 5-15 lbs each month for the first three months. Then the weight loss will slow to 2-5 lbs per month. However, 1/2-1 inch continues to disappear off the waist circumference measurement every month. THIS IS NORMAL. Continued weight loss of 15 lbs a month will leave you looking like the Michelin Tire Man – rolls of skin without fat. The body slows the weight loss to keep up with skin and connective tissue remodeling. As long as ketosis is maintained, the fat will continue to melt away. At this point, I’m not so worried about scale weight as I am your waist circumference.
Point of Focus: Successful ketosis does not always affect the scale, but usually causes your pants to fall down.
PRINCIPLE 6
It has been my experience that it takes about 18 months for the average patient to reverse the insulin resistance while following a carbohydrate-restricted, high-fat ketogenic lifestyle. There is no quick fix for this. If there was, I’d be sitting on a beautiful beach in the Caribbean.
Point of Focus: The Ketogenic dietary lifestyle is actually the antidote to insulin resistance, diabetes and the diseases of civilization.
PRINCIPLE 7
Improvement in insulin resistance has also been demonstrated with mild to moderate intensity resistance exercise. Moderate intensity resistance exercise is 20-30 minutes of exercise like walking, easy jogging, cycling, lifting weights, yoga or Pilates with speeds or weight heavy enough to break a sweat, but not so fast or heavy that you cannot carry on a conversation with your exercise partner. Exercise improvesinsulin resistance – BUT IT DOESN’T CAUSE WEIGHT LOSS! Yes, I know, Jack LaLanne just rolled over in his grave. But, let me say that again. Exercise improves insulin resistance, but it does not improve weight loss!! The three largest and most intensive studies of exercise involving over 67,000 people demonstrate that you can exercise till the cows come home and you’ll average about 1% weight loss. If you exercise, realize it WILL make you hungry. Eating the wrong food (carbohydrate containing foods) will stimulate insulin release causing your exercise to be fruitless (Actually, your diet should be “fruit-less” anyway)
Point of Focus: Exercise because you feel like it, it improves insulin sensitivity and it decreases stress, not for weight loss.
PRINCIPLE 8
If you are eating enough fat, you won’t be hungry. Although this doesn’t always hold true in the case of patient’s with lepin resistance. 40-60% of patients with insulin resistance have a concomitant leptin resistance (see the article on lepin resistance here). A ketogenic diet is one in which 50% or more of total calories come from fat. No, you don’t have to count calories, just pick foods that contain 45% fat or more. Look for grass fed products as they will be higher in Omega 3 fatty acids. Red meat is 55% fat. Pork is 45% fat. This is where the chicken salad or turkey wrap fails (see Why Does Your Chicken Salad Stop Weight Loss). Look for alternatives to replace your basic meals and snacks. If you love chips, try pork rinds or make chips from fried cheese or pepperoni. Guacamole is a great replacement for bean dip.
Point of Focus: There is no need to eat 3-6 times per day. As you increase the fat in your diet you will feel more full. Eat when you are hungry, whether that is 3 times a day or once day, listen to your body.
PRINCIPLE 9
I’ve been following a ketogenic diet for over 10 years. The most common complaint I hear is, “Dr. Nally, I’m tired of eating eggs.” Ketogenic diets don’t have to be boring. There are hundreds of resources on the web for spicing up your ketogenic diet. See the Recommended Sites page above for some ideas to start. The Ketogenic Cookbook by Jimmy Moore and Maria Emmerich is a recent edition to the literature and a fantastic resource. Check out Franziska Spritzler’s Low Carb Dietitian website and new book as well. If you live in the UK, you should see Emily Maguire’s website and blog. She just completed a world tour, sampling all the low carbohydrate foods and restaurants around the world. If you are a picture person, check out the Best Keto Meals of 2015 Pinterest page followed by almost 16,000 people. If you haven’t takent the time, you should visit Dr. Andreas Eenfeldt’s website. He is one of Sweden’s premier ketogenic doctors has an immense number of resources at his website, Diet Doctor. Finding someone that can help you fine tune your diet is also essential. You can find a list of doctors that use ketogenic diets here.
Point of Focus: This lifestyle will require you to use real, whole food and cook like your grandmother or great grandmother did in the past. Unfortunately, we’ve lost a great deal of the art of cooking that needs to be re-discovered. If your lifestyle is too busy to cook and prepare real food, that busyness is probably causing you stress, another culprit in the weight gain cycle. The truth will set you free, but it will probably make you miserable first.
PRINCIPLE 10
WARNING! A very sweet patient of mine was given these instructions to treat her weight and blood sugar abnormalities. She applied these principles and they worked marvelously. She called me a few weeks later, however, mad as a wet hen. She placed her husband (not my patient at the time) on the same dietary changes. Her husband, who had significant blood pressure problems and was on four different blood pressure medications I later found out, had a sudden drop in his blood pressure and passed out. As happens to many of my patients, blood pressure, ejection fraction of the heart and blood sugars quickly begin to normalize. However, he never saw his doctor and never had is blood pressure medications adjusted. Because of the normalization that can occur in as rapidly as 1-2 weeks, the medications became much too strong, he passed out and ended up in the emergency room. These dietary principles are effective. They are often just as powerful as a number of the medications that we routinely prescribe.
Point of Focus: Please see your doctor before beginning any of these dietary recommendations, especially if you have any underlying medical conditions including Hypertension, Diabetes, Congestive Heart Failure, Coronary Artery Disease, Gout, Kidney Stones, etc., please do not try the dietary changes alone. Find a physician trained in the use of this type of dietary lifestyle in combination with close monitoring of your blood pressure, blood sugar and other key vital signs.
Stay tuned for Ketogenic Principles . . . Part II in the series where we’ll address Food Psychology, To Cheat or Not to Cheat, and Keeping it Real . . .
I love chocolate chip cookies! However, over the last seven years, as I have followed a low carbohydrate diet I have not been able to indulge my chocolate chip cookie craving — until recently.
My gorgeous and very ingeniousness wife has perfected her chocolate chip cookie recipe and – Oh, WOW . . .are they good.
Warm, tasty chocolate chip cookies that are actually good for you, served up by a beautiful blond in a very cute apron. . . I think this is what heaven is like.
Low Carb Chocolate Chip Cookies
Here is a snapshot of the remaining batch my wife made at our house the other day before they got eaten. Boy, are they good. Here is the recipe:
Low Carbohydrate Chocolate Chip Cookies
1 tsp vanilla
2 eggs
2 sticks (1 cup) of butter, softened
1/2 cup Sweet Perfection
1/4 cup erythritol
1/4 cup Just Like Sugar (chicory root sweetener)
1 tsp salt
1 tsp baking soda
1 tsp baking powder
1 1/2 cup almond flour
1 cup coconut flour
1/2 cup Carbalose flour
2 ChocoPerfection Milk Chocolate bars chopped
Mix the vanilla, eggs, butter and sweeteners until creamy or fluffy. Add in all dry ingredients and mix. Add chocolate and mix. Place dough on parchment paper covered cookie sheets in 2 tsp sized scoops.
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).
If you are interested in the low-carb, moderate protein, high-fat, ketogenic diet, then 
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
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).
