Stomach Pain & Swelling with Hereditary Angio-Edema (HAE)
Listen to KetoTalk Podcast #32 where we talk about hereditary angio-edema, adequate ketone ranges, statin use while in ketosis and healthy keto questions. You can listen in by going to KetoTalk.com or you can listen in on iTunes.
“About 40 percent of my older patient population who take statins while eating ketogenic experience some form of myalgia they didn’t have before. And there’s an amplified side effect profile: muscle ache, joint pain, generalized fatigue, liver enzyme elevation, and cloudy headed.” — Dr. Adam Nally
What actually occurs in your metabolism when you become a fat burning machine?
How does functioning off of ketones aid and improve disease?
Join Dr.Nally online, via Webex, and learn how to optimize your body and your metabolism.
Ketogenic BioHacking with Dr. Adam Nally
Date: Wednesday, August 24, 2016
Time: 6:00 pm, Mountain Time (Arizona, GMT-07:00)
Session Number: 801 629 053
Registration password: Ketones
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To register for this training session click here:
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PLEASE NOTE: Registration for this even must be done on a computer. Once registered, the WebEx Workshop can be viewed on a computer, iPhone or iPad with.
Once you are approved by the host, you will receive a confirmation email with instructions for joining the session.
Too much protein, too little protein? How do you know how much protein to eat? This has become a very confusion question for many of my patients in recent years. There a a large amount of “mis-information” in the ketogenic world about the effect of protein of gaining and losing fat.
For the person exercising 5-6 days a week, 1 gram of protein per pound of ideal body weight is the formula that works quite well. However, for the average Joe or Mary who doesn’t work out for an hour a day 5 days a week, I’ve provided the calculation below. This calculation is a baseline starting point. It is the basic amount of needed protein to maintain muscle on a ketogenic or carnivorous diet:
Ideal Body Weight (IBW) is based on your height: Males: Protein in g/day of IBW = 50 g (for the first 5 feet of height) + 2.3 g for each inch over 5 feet. Then multiply the number you found by 1.2 (multiplier for sedentary male). [This lets you calculate the average male needs that are approximately 1.2 g of protein per kg of ideal body weight (IBW) per day.]
Females: Protein in kg/day of IBW = 45.5 g (for the first 5 feet of height) + 2.3 g for each inch over 5 feet. (This lets you calculate the average female needs 1.0 g per kg of ideal body weight per day.)
Example:
A 6 foot male’s protein calculation for IBW would be 50 g of protein (for the first 5 feet )+ 27.6 g (2.3 g x 12 inches) = 77.6 g x 1.2 = 93.2 g.
A 5 foot 4 inch females protein calculation for IBW would be 45.5 g (for the first 5 feet) + 9.2 g (2.3 g x 4 inches) = 54.7 g.
If you are exercising more than 60 minutes 5 days per week then the values above should be multiplied by 1.4 grams per kg for females and 1.6 grams per kg for males.
Heavy Exerciser Protein Calculation Example:
6 foot male’s base protein needs: 77.6 g per day (IBW calculated number before using the multiplier).
77.6 g x 1.6 = 124.5 g max
5′ 4″ female’s base protein needs: 54.7. g per day
54.7 g x 1.4 = 76.6 grams per day max
If you eat three times per day, then simply divide your protein needed for you IBW by 3 to get the maximum protein you need per meal.
Come join us on August 4th at 7pm for an evening of fun filled learning about health, diet and how ketones play a role in a healthy lifestyle. Get a chance to talk with Dr. Nally and try out a sample of exogenous ketones.
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 the blogosphere, and our two amazing co-hosts are shooting them down one at a time. Keto Talk is co-hosted by 10-year veteran health podcaster and international bestselling author Jimmy Moore from “Livin’ La Vida Low-Carb” and Arizona osteopath and certified obesity medicine physician Dr. Adam Nally from “Doc Muscles” who thoroughly share from their wealth of experience on the ketogenic lifestyle each and every Thursday.
KEY QUOTE: “Children are born in ketosis, so ketones are perfect for babies. The level of fat in breast-milk is essential for them to maintain their health and their growth.” — Dr. Adam Nally
Here’s are the 12 questions Jimmy and Adam answered in this special Keto Talk Mailbox Blitz extended podcast today:
– Testimonial from someone who learned his lesson why it’s important to stay ketogenic all the time
– Three-decade study confirms saturated fats are bad for health
– Is increased testosterone from a ketogenic diet a bad thing for women?
– Why am I still struggling with low energy and low ketones after months of being in ketosis?
– Can being in nutritional ketosis above 1.0 mmol cause painful headaches?
– Do artificial sweeteners and stevia raise insulin?
– Is my ketogenic diet causing me to cramp up before and during my half marathon racing?
– Is MCT oil a better fat to use on a ketogenic diet than other fats like coconut oil, cream, or butter?
– Why do I have a constant stomachache while I’m on a ketogenic diet?
– Do you have to be in ketosis to burn fat?
– Does being in ketosis lead to daily spotting and extended periods?
– Are ketones in my baby’s breastmilk safe for her to consume? And why did my milk supply drop when I went keto?
– What is the impact of the supplement creatine on ketones, blood sugar, and insulin levels?
– Can I ease into ketosis as a way to avoid the dreaded “keto flu?”
KEY QUOTE: “If you’re not feeling energy after that adaptation period of 2-4 weeks at the very most, then you’re doing something wrong. Let that be your wakeup call to change something.” — Jimmy Moore
Hypertension (elevated blood pressure) is one of the triad symptoms of metabolic syndrome. Most of the hypertension that I see clinically is driven by insulin resistance as the underlying cause. I see this problem in a very large majority of the people in my office and I am seeing people younger and younger show up with continually increasing blood pressure.
In medical school, we were taught to treat “borderline” or “slightly elevated blood pressure,” through “lifestyle changes” which was another way of saying exercise, caloric restriction & hold the salt. But most physicians today will tell you that exercise, salt & caloric restriction doesn’t work. When asked why the 34 year old male in my office suddenly has elevated blood pressure, the only explanation we had was it is a “genetic problem,” or “blood pressure naturally goes up as we get older,” or “you’ve been eating too much salt,” and they are started on blood pressure medication and sent on their way. But, as time went on, I found that I had to keep adding more and more blood pressure medication to control the continually rising blood pressure of the patients in my practice.
Most of these people will have a progressive elevation in blood pressure over time, and these blood pressure (anti-hypertensive) medications are/were continually raised until the person is on four or five different blood pressure pills at maximal doses. Again, when questioned why, their genetics are blamed and that is the end of it. Or is it?!
What shocked me was that when I took patients off of salt & caloric restriction, and placed them on low carbohydrate high fat diets (and yes, I gave them back their salt), their blood pressure normalized. I noticed that as their fasting insulin levels began to fall, their blood pressure began to return to normal.
What?! Blood pressure rise is caused by insulin?!
Ummm . . . Yes!
I am a prime example. During the first few years of my medical practice and reserve military service, we had routine vitals checkups. I was working out 3-5 days a week with weights and running 3-5 miles 2-3 times a week and restricting my calories to 1500 per day. So, I thought I was in pretty good shape. However, it was not uncommon for for the nurse to raise her eyebrows at my blood pressure readings in the 140-160 systolic and 85-98 range diastolic. “Oh, it’s the lack of sleep last night,” or “it’s the caffeine I had this morning,” would be my excuse. But I was making a lot of excuses, and in light of those excuses, my caloric restriction, exercise and salt restriction, I was also still gaining weight.
By the 5th year of my medical practice, I weighed 60 lbs heavier than I do today and I struggled to keep my blood pressure under 150/95. I was violating my own counsel . . . don’t trust a fat doctor for nutritional advise. (Or, was that advise from Dr.House?)
A much slimmer, healthier and happier Dr. Nally (center) in 2016
After cutting out the carbohydrates (I’ve kept my carbohydrate intake < 20 grams per day), moderating my protein intake and eating all the fat I am hungry for each day, my recent physical examination at the beginning of June 2016 revealed my blood pressure at 112/64. I don’t remember ever having blood pressure that low. And to be honest, I didn’t sleep well the night before my exam due to a number of middle of the night patient calls.
When I first started treating the insulin resistance problem in the human, rather than the blood pressure problem, I began to see immediate reductions in blood pressure within one to two weeks. So much of a reduction that if I didn’t warn the patient that they should begin to back down their blood pressure medications, they would experience symptoms of dizziness, light-headedness, headache and a few patient’s nearly passing out. On a low-carbohydrate, high-fat (ketogenic) diet you need salt (sodium, potassium, & magnesium). The process of burning fat as fuel causes you to lose increased amounts of sodium & potassium, and you have to replace these electrolytes. A number of my patients begin a low-carbohydrate, high-fat diet and are afraid of increasing their salt intake. Not replacing these electrolytes while on a ketogenic diet can also lead to low blood pressure, dehydrate and dizziness.
I often wondered why applying a ketogenic diet had such a profound effect on blood pressure so quickly. Dr. Robert Lustig helped answer that question for me.
In order to understand how the Standard American Diet (we call it the SAD diet in my office) raises your blood pressure, it is important to understand how the body processes the basic sugar molecule. Sugar is one glucose molecule bound to a fructose molecule. This is broken down in the body and 20% of the glucose is metabolized in the liver, the other 80% is sent on to be used as fuel throughout the body. Fructose, however, is where the problems arise. 100% of the fructose is metabolized in the liver, and the by product of fructose metabolism is increasing the liver’s production of MORE glucose and the byproduct of uric acid. Uric acid is produced and this inhibits the production of nitric oxide. The diminished nitric oxide in the presence of an increased level of glucose (stimulating increased insulin production due to eating starches) constricts the blood vessels and raises blood pressure. Yes, that donut you just ate raised your blood pressure for the next 12 hours.
The mechanism that fructose containing carbohydrates, sugars and starches raise blood pressure, cholesterol and cause weight gain can be seen in the really complex diagram found in Dr. Lustig’s 2010 article:
So, how do you lower your blood pressure through diet?
First, cut out all the simple sugars. These include anything with table sugar, high fructose corn syrup and corn syrup. (This is why people with any change in diet see some improvement in weight and blood pressure as they remove the simple sugars like candy, sugared drinks and pastries from their diet.)
Second, limit your overall intake of other sources of carbohydrates including any type of bread, rice, pasta, tortilla, potato, corn and carrots. Realize that carbohydrate in fruit is fructose, and when taken with other forms of glucose can have the same effect as table sugar – it can and will raise your blood pressure, as well as halt or cause weight gain.
Third, if you are taking blood pressure medications for hypertension, see your doctor about close monitoring of your blood pressure as it can and will drop within 2-4 weeks of making these dietary changes.
Maintaining ketosis is really important for weight loss and blood pressure or hypertension control. I am very much an advocate of using real food for this process, but I have also found that the use of exogenous ketone salts aid significantly in maintaining ketosis. I have found that exogenous ketones are the next step in bridging the difficulty of day to day maintenance of ketosis.
It isn’t making the mistakes that’s critical; it’s correcting them and getting on with the task that’s important. If you’ve been calorie restricting and exercising to lower you blood pressure, don’t fret. A simple change in your diet focused on restricting starches and carbohydrates has been demonstrated in my office to be more powerful than many of the blood pressure medications we’ve used for years.
Over the last few months, I’ve found myself amid the center of vehement nutritional arguments about fat, carbohydrates, calories and diet. I have found it fascinating that very intelligent men and women, over the last 50 years, have accepted, without reservation, a dogma taught them by their eighth grade nutrition teachers. This dogma is interlaced and interwoven throughout the textbooks, manuals, and college cafeterias throughout the world.
It is a well known fact, however, that hydrogen is the most common element in the universe and is used as a basic building block for most molecular structures. What many don’t realize is there exists another element yet to be added to the periodic table that is almost as prevalent called moronium (pending symbol approval – Mu). It fills the blank space on the table of elements between Hydrogen and Helium. I, and those who have been able to identify this element, suspect that moronium is a gas at room temperature and has some affinity to binding the white matter of the brain responsible for catechol-O-methyltransferase (COMT) gene regulation of the prefrontal cortex. It is suspected by some that when it is inhaled by a person of low intellect, it has only a mild effect. However, when combined with either oxygen (O), hydrogen (H) or Helium (He) and inhaled by those of higher intelligence, it has a much wider, more potent and even stupefying diffusion effect, that is quite surprising to witness.
Moronium reacts adversely when diffused into blood with a higher alcohol concentration and seems to spontaneously combust when it is exposed to old paper and libraries. Moronium is very difficult and very expensive to isolate. Moronium seems to be more prevalent during the summer and winter solstices, which may be why moronium intoxication seems to appear around holidays. Recent attempts in a nearby lab to synthetically create even small crystals of moronium cause an explosion, physically and psychologically stupefying all of the researchers involved and inducing them to leave the study of science and pursue individual careers as drummers.
The presence of moronium seems to be higher in those that do not read, or have an aversion to reading. There is some correlation that moronium drops in proportion to listening to iTunes podcasts, however, follow-up reading does appear to have a potential lowering affect on the moronium levels within the brain.
Why do I bring this up?
I suspect that this little known element may be responsible for intelligent men and women introducing questionable theoretical science as incontrovertible truth. Those with suppressed COMT regulation seem to have a propensity to accept theoretical science because it sounds good, even when there’s really no way to actually prove the theory at the time, or when colleagues have accepted the theory in a peer-pressure instead of peer-review situation.
The stupefying effect of moronium bound COMT produces dogma like:
Miasmatic Theory of Disease (A noxious poisonous vapor of air called miasma filled with decomposed particles of matter believed to be the cause of cholera and chlamydia or the Black Death)
The amazing thing about science is that it is self-correcting (at least it used to be). A scientist makes a set of observations about nature, and then identifies a plausible theory within the laws of nature to fit those observations. Then, researchers take that theory and test it in as many ways as possible, attempting to disprove the theory and isolate the cause of the observation. If the theory withstands scrutiny it becomes widely accepted.
At any given point in the future, if contradicting evidence emerges, the original theory is discarded and a new theory is then identified. In essence, this is the simple scientific method, however, in modern day application, it has become a great deal more messy than you’d think.
This approach (application of “the scientific method”) was skirted during the 1960’s and 1970’s regarding the “fat causes heart disease” theoretical proposition. Interestingly, there was also a notable increase in the number drummers and musicians during the 1980’s Hair Bands era. This begs the questions, which I wholly agree needs further study: Does moronium exist? and . . . . Did levels of moronium actually increase between 1960 and 1990 causing a surge in the presence and popularity of Hair Bands?
It only took us 20 years to get past the Era of the HairBands, hopefully we can turn the nutritional ship around and recognize the real culprit causing the Diseases of Civilization.
Ketosis in 60 minutes . . .
The Multi-Vitamin Dr. Nally Personally Uses
(Author’s Note: For those who may possibly be under the influence of moronium toxicity, the post above is written in sarcastic jest, and to be clear, there IS NOT an element currently under investigation called moronium!)
Dr. Nally recently spoke about Low-Carbohydrate/Ketogenic Diets on the 2016 Low Carb Cruise to the Eastern Caribbean. While there, he and Jimmy Moore recorded another episode of KetoTalk with Jimmy and the Doc.
Here’s what Jimmy and Dr. Nally talked about in Episode 20:
– We are in front of a LIVE audience of Ketonians
– How long will you experience hair loss when you go ketogenic?
– What role does resistant starch have on the keto diet?
– Is eating high-fat with high-carb harming my boyfriend?
– How does intermittent fasting help with keto?
– Whether to count total vs. net carbohydrates
– Whether you need to cycle carbs when building muscle
– What the best way to test your ketones is
– How to test blood ketones on a budget
– What the difference is between an NMR and basic lipid panel
– The dramatic changes in your cholesterol when going keto
– How long should you be on keto before running blood tests?
– Whether you should cut fat lower on keto to speed up weight loss
– Is having a lower body temperature a bad thing when eating keto?
You can listen at the iTunes page here, or download it for free to your favorite iTunes player.
Alzheimer’s disease puzzle pieces now starting to fit
Alzheimer’s Disease is a progressively devastating, fatal disease that affects 5.2 million Americans and over 44 million people throughout the world. This disease is often more difficult on the families and caregivers, then on the patient’s themselves. With my office located near three of the country’s largest retirement communities, it is a disease that I see and treat every single day.
A paper published in the Journal of Alzheimer’s Disease this week, confirmed suspicions and patterns that I have been seeing for over 15 years. A significant number of my patients with Alzheimer’s dementia (AD) also have insulin resistance, impaired fasting glucose or diabetes mellitus – type II. I have long wondered if there was a tie to these diseases because of the patterns seen in my office. However, much of the research examining the association between type II diabetes and AD have come to differing conclusions about the cause. Some have concluded that insulin resistance is to blame and others have concluded that insulin deficiency may play a role. Other studies have found that a hormone called amylin secreted with insulin is to blame. And, other articles have found that both amylin and amyloid-beta protein form the plaques within the brain common to AD. Lastly, more recent data complied appears to point to the opposite conclusion – that amylin provides neruro-protective effects and may actually reduce the symptoms of AD. So, what are we to make of all of this? How is the doctor in the trenches to interpret and then advise those with or at risk for Alzheimer’s Disease?
The paper referenced above, by Dr. Schilling, takes all of this data into account and with careful attention to research methods and compiling immense amounts of data from all of these studies, it identifies the integration points with insulin and insulin-degrading enzyme (IDE) that have begun to disentangle the research. What it reveals is fascinating information.
First, under normal circumstances, we now know that insulin stimulates the expression of IDE, which subsequently breaks insulin down after it is used. IDE, however, also plays a roll in breaking down amyloid-beta protein and other amyloidogenic peptides. Alzheimer’s disease is caused by a build up of these amyloid based proteins forming plaques within the human brain.
Second, the body’s system for breaking down and removing these plaques can fail or become inefficient in four different ways. What has been confusion for many years to researchers is now much more clear with our clarified understanding of insulin resistance moving through five different stages (see my article on Diabetes Mellitus type II – really the fourth stage of insulin resistance).
What are these four possible points of breakdown?
In the fifth or last stage of insulin resistance (where insulin deficiency occurs due to pancreatic failure and lack of adequate insulin production) or in a type 1 diabetes patient who makes no insulin at all, inadequate IDE can result in accumulation of amyloid-beta in the brain. Poor IDE production may cause amylin and amyloid-beta plaques in the brain.
Diminished IDE production due to any other cause may lead to amylin and amyloid-beta plaque formation leading to AD
Excessive production of insulin, occurring in stages I-IV of insulin resistance, stimulates increased amylin production which competitively inhibit breakdown of amyloid-beta resulting in AD.
Production of more than the typical level of amyloidogenic peptide that outpaces the formation of IDE is the fourth mechanism occurring with insulin resistance and stimulates the formation of amyloid plaque in the brain consistent with AD.
Further study is essential to tease out what the nuts and bolts of the mechanism may be, but with our understanding of stages of insulin resistance, the puzzle pieces are falling into place. This conglomeration of data provides further confirmation that insulin resistance is likely the key player in the progression of Alzheimer’s Disease years before type II diabetes or type I insulin dependence are ever diagnosed in the individual.
What is the take home message today? Impaired fasting glucose, diabetes mellitus and Alzheimer’s disease are later expressions of the underlying problem: insulin resistance. This is where a low carbohydrate and/or ketogenic diet begins to play a huge role in both prevention and treatment of Alzheimer’s Disease.
More to come . . . In the mean time, pass the butter and the Keto//OS.
As I reviewed my website recently, I realized that I have posted lots of science but I’ve never posted any success stories. So, as patient’s are comfortable & willing to share, I will begin posting these experiences here on the blogosphere for the world to witness their successes and the power of the KetoDynamic Antidote.
The first success story is my own. This picture of me and my wife, were taken after I had been following a ketogenic lifestyle for about 4 years. I dropped 60 lbs, normalized my cholesterol and blood sugar also normalized. I couldn’t and wouldn’t recommend these lifestyle changes unless I was willing to follow them for the long haul myself. I call people following a ketogenic lifestyle for longer than a year “Ketonians.”
Not only mine, but hundreds of patient’s having similar successes have become the greatest reward to my career as a physician over the last 15 years. They are truly the “KetoDynamic Moments” that etch themselves into my memory and have made me such an advocate of a ketogenic lifestyle. Therefore, it is with great honor and excitement that I have been allowed to share Michelle’s story below.
Michelle started seeing me in October 2015. She has struggled with weight all her life and, now in her late 40’s, weighed 201 lbs with a waist circumference of almost 36 inches and a body mass index of 32. Her “before” picture was taken just before a Halloween activity in 2015. Her “after” picture was taken in late March 2016.
A simple ketogenic lifestyle change ( <20g of carbohydrates, moderate protein for her ideal body weight & increasing fat to > 60% of total calories) has produced almost 50 lbs of weight loss and 6 inches off her waist in just 5 months. This was with dietary change only (Michelle doesn’t exercise) and she’s still losing weight. What is dramatic, and I see it every day, is that Michelle looks younger by at least 10 years (she actually added 20 years to her life span with this weight loss already). She feels fantastic. Blood sugar and cholesterol are now under control and she has tremendous amounts of energy. Her picture in March is at a body mass index of 29.
Michelle doesn’t calorie restrict. She just eats until she is full. Congratulations, Michelle!!! And, keep up the great work.
If you’d like to share your KetoDynamic successes with me and my audience, please let me know.
A patient recently asked me how bad being in nutritional ketosis was for her. I responded that the worse problem I’ve seen recently is the patient that broke his toe when he slipped on bacon grease. Are there risks with a ketogenic diet? Yes, but these usually only occur when you cheat or fall off the wagon. What problems can arise? Lets talk about them individually.
First, as I stated above, make sure you don’t slip on bacon the grease. It really can be an issue if you’re not used to using increased amounts of fat in your kitchen. So, be prepared for how to cook and use fat. Grandma understood this well, we could learn a great deal from her if you ask her about using bacon grease.
Second, let’s define the difference between ketosis and keto-acidosis and try to clarify the misinformation that is being spread around the blogosphere.
A ketone is a molecule the body produces from the breakdown of fat (specifically triglycerides) and some proteins (amino acids). There are specifically three types of ketones: beta-hydroxybutyric acid, acetoacetic acid and acetone. If ketosis was “bad,” then why would our bodies produce these molecules? They are not bad, and in fact, multiple studies show that the body is often more efficient in weight loss, inflammatory reduction, bowel function, epigenetic influence and maintenance of lean body mass more effectivly when it functions on ketones rather than glucose as its primary fuel source. You can see these studies here, here, here and here.
The body can only supply a limited amount of sugar or glucose for fuel. If you talk to runners, marathoners or triathletes, they will tell you that after about 45-90 minutes of continuous endurance exercise the glucose supply runs out and they will experience what is termed a “bonk” (have a low-blood sugar or hypoglycemic episode). Unfortunately, our bodies can only store about 18-24 hours of glucose.
However, the body can store days upon days of fat in the form of triglyceride in the fat cells. Triglyceride is broken down into ketones. If glucose is the “unleaded” fuel, you can think of ketones as the “diesel fuel” that is easier to store and runs longer.
The average body functioning on ketones as the primary fuel will have a ketone level measured in the blood somewhere between 0.4 and 4 mmol/L. Because of a balance that is created by the use of ketones and a feedback mechanism that kicks in when the ketone level rises, the body will maintain a pH of around 7.4.
Ketoacidosis is dramatically different. If you are a type I diabetic, you don’t produce any insulin. The feedback mechanism regulating ketone use is broken and the ketone levels and triglyceride breakdown speeds up because the body can’t access glucose and can’t produce insulin. The ketone levels spike and the level can rise to > 25 mmol/L. In the presence of a high blood sugar and high ketone level, the acid level in the blood shifts to a pH of less than 7.3. This is referred to as metabolic acidosis and can be life threatening as the low pH shuts down the bodies’ enzymatic processes and a person becomes critically ill and without treatment, can die. Further information on ketoacidosis can be found here.
If you’re not a type I diabetic, you have nothing to worry about. Regardless of what the “ketogenic nay-sayers” blog about, your liver makes approximately 240g of glucose per day, 24 hours a day, 7 days per week, this stimulates a basal release of insulin which keeps the pH in check. It’s also what keeps weight loss at a consistent pace of around 2-10 lbs per month.
If you are a type I diabetic, don’t fret. Carbohydrate restriction can still be used very effectively. It just takes some balancing and understanding of your individual metabolism. It does require close blood sugar and insulin monitoring. If you are a Type I diabetic, please talk to your physician, obesity specialist and/or bariatrician about how to follow a carbohydrate restricted diet while using insulin. It can be done and it can be done very effectively, but monitoring is essential.
What are the other potential problems that can arise when you follow a ketogenic diet?
Gastrointestinal (GI) Disturbances – Yes. Any time you change your diet you may experience diarrhea, constipation or gassiness. Most of the time, this is because you are either 1) not eating enough leafy greens (fiber) or 2) you’re using a supplement that contains an artificial sweetener. Most of the studies on ketogenic diets did not incorporate fiber and the studies used to make this point were on children who used a ketogenic fat supplement shake or liquid preparations containing these artificial sweeteners to make them palatable. If you have spoken to any obesity specialist, they will tell you, the best way to follow a ketogenic diet is to eat real food. If you want to read about the anecdotal GI effects of sweeteners, read the comment section in Amazon about the Haribo Sugar Free Gummy Bears.
Oh, by the way, 65% of patients in my practice following ketogenic diet see improvement in gastroesophageal reflux (GERD) symptoms. This was seen in a 2006 study looking at ketogenic diets and reflux.
Hair Loss/Thinning– Yes. This does happen initially and if you are not eating enough fat. It is important to note that hair loss/thinning can occur with any form of weight loss. You can see data on this here. Hair loss is very common if you are restricting calories, which was occurring in a number of the ketogenic dietary studies previously published. You do not, and should not, need to “restrict calories” if you are following a ketogenic diet correctly, and in fact, most people take in more than 1800 calories on a ketogenic diet.
Inflammation Risk– In every patient that I have placed on a ketogenic diet in the last 10 years, all inflammatory markers including CRP, Sedimentation Rate, Apo B, HOMA-IR and Uric Acid have all decreased. Inflammation gets better on an appropriately formulated ketogenic diet. The older studies of ketogenic diets in children contain most of their fat from Omega-6 fatty acids from vegetable oil which will increase inflammation and oxidative stress, spike the cortisol levels and have the secondary effect of actually raising the triglycerides. You can find more information on this here & here.
Kidney Stones/Gout – These (kidney stones & gout) are both commonly caused by spikes in uric acid. As noted above, I’ve seen multiple cases in my practice where a ketogenic diet lowers uric acid. Only a small clinical trial has been published in the literature (and it wasn’t truely ketogenic), but the results point to the potential for ketogenic diets to lower uric acid. Ketogenic diets also have the capacity to lower the formation of calcium oxalate stones through a secondary mechanism where calcium oxalate formation is driven by uric acid formation. Older small case reports in the pediatric seizure literature identify calcium oxalate stones, however, dehydration (too little fluid/water intake) is the primary cause of kidney stones.
So, are ketogenic dietary patients at risk? Only if you cheat on your carbohydrate restriction and you let yourself get dehydrated. So, I warn patients. Don’t cheat and make sure your drinking adequate amounts of water.
Muscle Cramps/Weakness– The process of weight loss occurs by burning fat into CO2 and water. We breathe the CO2 out, but the water produced has to follow salts out through the kidneys. Hence, we lose water and salts. This can cause weakness and muscle cramps. The solution? Stop restricting salt on a low carbohydrate diet. We are the only mammal that restricts salt and we do it because low-fat diets cause us to retain water. Low carbohydrate diets do the opposite. Use sea salt or sip beef or chicken bouillon broth with your dinner. You may consider adding magnesium to your diet. The use of yellow mustard also helps (the small amount of quinine in yellow mustard stops the cramping). If you have congestive heart failure, talk to your doctor about monitoring your salt intake in balance with your diuretic or water pill.
Hypoglycemia– If you read the ketogenic diet research, most of it was done on epileptic children. The diets called for a period of starvation, and then the introduction of a ketogenic liquid based shake following the John’s Hopkin’s protocol. It is a well-known fact in medicine that starvation in children can frequently cause hypoglycemia, especially in children with other genetic or congenital defects leading to forms of epilepsy. In clinical practice, with ketogenic diet use in adults, hypoglycemia is rare. The only time I see hypoglycemia is when patient’s with significant insulin resistance or diabetes cheat on a large amount of carbohydrate and get a secondary insulin surge leading to hypoglycemia 3-5 hours after cheating.
Low Platelet Count (Thrombocytopenia)– Again, this was seen in epileptic children who were placed into starvation first, then introduced a liquid fat replacement shake to stop intractable seizures. These liquids or shakes were often nutrient deficient in other essentials. Folic acid, B12 and copper deficiency can occur when not eating “real food.” Low platelet counts are rarely seen on ketogenic diets based around “real food.” Many children in the ketogenic studies had been on or were concomitantly on valproic acid for their seizures. Valproic acid is commonly known to cause thrombocytopenia and this is another reason that thrombocytopenia was seen in this population. (Barry-Kravis E et al, Bruising and the ketogenic diet: evidence for diet-induced changes in platelet function. Ann Neurol. 2001 Jan;49(1):98-103.; Kraut E, Easy Bruising, http://www.uptodate.com, May 2015.)
Impaired Concentration/Mood– A number of patients starting carbohydrate restriction will go through 2-4 weeks of carbohydrate withdrawal. This carbohydrate withdrawl can be experienced just as powerfully as morphine withdrawal in some patients. Sugar is a drug and has a powerful effect on the same hedonic receptors that morphine does in the brain. Some patients will experience headache, tremor and decreased concentration while “withdrawing” off of starches and carbohydrates. Studies show that after the 4-8 week period of keto-adaptation, cognitive function dramatically improves.
Easy Bruising – This is usually due to inadequate protein supplementation as was the case in much of the ketogenic literature where protein levels were also restricted. (Kraut E, Easy Bruising, http://www.uptodate.com, May 2015.)
Pancreatitis – Patients who are insulin resistant or have impaired fasting glucose commonly have high triglycerides. Elevation in triglycerides itself is a cause of pancreatitis. Ketogenic diets lower the triglycerides. However, if a patient has not been following their diet as directed, spikes in the triglycerides can occur placing the person at risk for pancreatitis.
Long QT Intervals/Heart Arrhythmias – The list of things causing Long QT intervals and abnormal heart rhythms is long and variable (Acquired Long QT Syndrome. Berul C et al. www.uptodate.com, May 2015). It is well know that starvation, rapid weight loss and liquid protein diets can cause a delay in the conduction signal in the heart. Anyone wishing to start any diet should have an electrocardiogram (EKG) through their doctor to ensure that the diet (of any type) doesn’t exacerbate a prolonged QT interval.
Cardiomyopathy– Prolonged QT intervals have been associated with cardiomyopathy and the former can stimulate the later. Any diet that has the potential to prolong a QT interval has the potential to cause cardiomyopathy. Hence the need for regular EKG monitoring on any diet (Acquired Long QT Syndrome. Berul C et al. www.uptodate.com, May 2015).
Lipid/Cholesterol Changes – In the 10 years I have been prescribing ketogenic diets to patients, I have seen dramatic improvement in the triglycerides, small dense LDL particle and HDL levels. The only time triglycerides rise over 100 is if the patient is using artificial sweeteners, is cheating on the carbohydrate restriction, or is taking in too much protein. Total cholesterol commonly rises, however, this is indicative of the fact that there is a shift in the LDL particle size and this affects the calculation of both total cholesterol and LDL-C. In light of this, most of my patients have dramatic improvement in triglycerides and small dense LDL particle number.
Myocardial Infarction – In older papers, elevated total cholesterol was noted and the authors made the “assumption” that myocardial infarction “could” be a risk. We now recognize that elevated Total Cholesterol is NOT a causitive risk for heart disease.
These previous assumptions have been interpreted by the blogosphere ketogenic “nay-sayers” as actual risk. However, a correlation and causation was never made. Again, in the 10 years I have been using and prescribing ketogenic diets, I have seen dramatic improvement in cholesterol profiles, inflammatory markers, atherosclerosis and carotid intimal studies (Shai I et al, Circulation 2010; 121:1200-1208).
Menstrual Irregularities / Amenorrhea– It is well known that any diet causing protein or other nutritional deficiency will affect the menstrual cycle first and growth in stature second. The only time menstrual irregularities occur with a ketogenic or Low-Carb diet is when a patient is not taking in enough protein and/or fat, and is not eating real food. What amazes me is that a properly applied ketogenic diet actually causes normalization of the menstrual cycle, and in my practice, I’ve had a number of women successfully be able to conceive after making a ketogenic dietary change.
Is a ketogenic diet bad for you? You be the judge.
If you are following a ketogenic diet correctly and with real food, the only thing you really need to worry about is slipping on bacon grease.
In an era where over 70% of us (35.7% obesity & 34% overweight in 2015 according to the CDC) have started to resemble the food pyramid, seeing the effect of a carbohydrate heavy diet should give a clue.
Our bodies were meant to burn ketones. We have a parallel system within us designed to use ketones as an energy source. Ketones are faster and more efficient than the way our bodies use glucose. Ketones give you 38% more energy than you can get from glucose. We as a society are following a deceptive food pyramid.
When we limit or remove carbohydrate from our diet, we are left with ketones as a primary fuel. It is time that we recognize what Dr. Yudkin was trying to tell us in 1970’s, that our carbohydrate and sugar intake is the driver for heart disease, diabetes and the diseases of civilization. (Yudkin, John. Sweet and dangerous: the new facts about the sugar you eat as a cause of heart disease, diabetes, and other killers. PH Wyden, 1972.)
Ever wondered if it is possible to change up your metabolic genetics for the better? Come join me this week. I’ll be speaking about Ketogenic BioHacking, Thursday, March 31st, in Scottsdale, Arizona. Meet me from 7-8:30pm and learn how to improve fat burning, bio-hack your epi-genetic metabolism for improved blood sugar, cholesterol, blood pressure and so much more . . .
You’ll also get to meet Kim Minert who will be signing her new book, Burn Fat for Fuel. And, you’ll get a chance to meet the amazing Abigail Epps-Kluttz, body builder, fitness model & Pruvit Ambassador.
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.
Listen to Jimmy and me answer rapid fire KetoTalk Mailbox questions for a solid hour on our most recent (released today) KetoTalk podcast #14 (available on iTunes). This was a fun podcast. I hope you enjoy it as much as I did recording it.
I am a family physician. Each door I open holds another challenge, another question or another puzzle. You never know what will be behind door number 2 or number 3. This leads to becoming very adept at understanding and thinking about the random. Door #1 one holds the rash. Door #2 holds the patient with diabetes. Door #3 . . . rectal bleeding. Yes, my morning often starts out just that way.
While randomly thinking about the randomness that my career choice brought to my life, I’ve made a few random decisions that relate to our health in general.
First, if I ever decide to buy a toilet paper roll company, I’ve already made the executive decision that each piece of paper on the roll needs the opportunity to express itself in a random way. One piece would say, “Nice fingernail polish.” Another would say, “Wow, you have a nice bottom.” A third would say, “Please don’t apologize, brown is my favorite color.” A fourth might say, “You know, you really should see your doctor about that . . . ”
Second, if I live until I’m 70 years old, I will have spent 10 of those years on Monday. This calls for sausage and eggs for breakfast every Monday morning. Wait, I’m already doing that . . . no wonder I like Mondays. It also means that if I set my clock to wake up earlier on the weekend, then Monday morning I will start the week off “sleeping in.” It is amazing to me that even under ideal conditions people have trouble locating their car keys in a pocket, finding their cell phone, and even pinning the tail on the donkey . . . but I’d bet everyone of us can find & push the SNOOZE button from 3 feet away, in about 1.7 seconds, eyes closed, first time, every time…
Third, with all of this randomness . . . someone needs to invent the “Sarcasm Font.” There are some things that shouldn’t be written in “Times New Roman.”
Fourth, Can I take back all those times I didn’t want to take a nap when I was younger? I am quite convinced that a significant number of my obesity patient’s would be so much more successful with an afternoon nap.
Fifth, in the age of computers, voice recognition, iPhones and electronic medical records, I really want to meet the person that invented cursive and ask, “Was that really necessary?”
Sixth, in this new era of reality everything, I think that print newspapers would still be fascinatingly successful if the obituary column told you how the person died.
KetoOS – Drinkable Exogenous Ketones
Seventh, with all the high fat, moderate protein I recommend, the freezer has become an important appliance in the ketogenic world . . .yet no one can answer me this question: “Why is there still no freezer light?”
Last, bad decisions often make for the best stories. . . .
“But I don’t understand why I still feel this way . . .”
I hear this every day.
Sometimes we have to dig deep for the answer, sometimes it’s just the act of listening that helps us find the answer and sometimes it’s the nail staring us right in the face. We often don’t want to recognized patterns in our lives that adversely affect us because we’ve become comfortable with those patterns.
Is that piece of toast, that piece of fruit, that creamer in your coffee, that bowl of cereal or is it really the nail?
Sometimes, you don’t need to be fixed . . . you just need to be heard.
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!
(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.)
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:
It has long been understood that tumor cells of any kind require high levels of glucose to grow and spread (1,2). It is also recognized that higher levels of insulin, commonly found in patients with insulin resistance or type II diabetes, are 2.4 times more likely to stimulate the development of breast cancer (3). A diet low in glucose has thereby been theorized to be an adjunct to cancer treatment.
Ketogenic diets have been demonstrated to be therapeutically useful in the treatments of epilepsy and cardiovascular disease (4). A ketogenic diet is one in which carbohydrate levels are kept below 50 grams per day and fat intake is increased to the point that the body shifts its metabolism to use triglycerides, and the ketones derived from triglycerides, as the primary fuel source for the majority of the cells within the body. With this understanding in mind, the application of a ketogenic diet, one high in fat and protein with limited carbohydrate or glucose has been suggested as a adjunct to cancer treatments (5).
KetoOS – Drinkable Exogenous Ketones
A recent study (6) in the Oncology Letters evaluated the benefits of a ketogenic diet in 78 cancer patients in clinical practice. A novel marker measuring the tumor cells use of glucose called transketolase-like-1 (TKTL1) was closely monitored, as was each of the 78 patients adherence to a ketogenic diet. Increased TKTL1 was noted in more aggressively active and growing tumors (7,8).
Among the 43 males and 35 females, 7 patients agree to and followed a fully ketogenic diet and 6 of them followed a partially ketogenic diet. Ketogenic meals were provided by a German company called Tavarlin that would prepare and mail ketogenic meals including oil, fat, snacks, bread, protein and energy drinks. Dietary journals were reviewed every three months over a period of about 10 months.
40 % of these patients experienced a halting of the tumor progression and 60% experienced improvement noted by normalization of TKTL1 or reduction in TKTL1, respectively. Those on a ketogenic diet demonstrated an average reduction of TKTL1 by approximately 50%.
This is the first study of its kind and has significant potential. Could dietary carbohydrate restriction be an effective cancer treatment or adjunct to cancer treatment?
Because the food diaries were based on reporting only, the sample study was very small, and patients treated in the outpatient setting have the possibility of variability in the standard oncologic treatments, the results must be interpreted with caution. However, the data is very promising. This study is one in which I have great interest as I have seen similar results in my clinic on a case by case basis.
Based on the limitations noted above, rigorous randomized control studies are needed, but this is an exciting an promising first step. Additionally, the presence of a marker for tumor growth that correlates with diet is remarkable. And, it provides the ketogenic specialist a possible measurement tool that could be used clinically.
References:
Klement RJ and Kämmerer U: Is there a role for carbohydrate restriction in the treatment and prevention of cancer? Nutr Metab (Lond) 8: 75, 2011
Vaughn AE and Deshmukh M: Glucose metabolism inhibits apoptosis in neurons and cancer cells by redox inactivation of cytochrome c. Nat Cell Biol 10: 1477-1483, 2008.
Gunter MJ, Hoover DR, Yu H, Wassertheil-Smoller S, Rohan TE, Manson JE, Li J, Ho GY, Xue X, Anderson GL, et al: Insulin, insulin-like growth factor-I, and risk of breast cancer in postmenopausal women. J Natl Cancer Inst 101: 48-60, 2009.
Paoli A, Rubini A, Volek JS and GrimaldiKA: Beyond weight loss: A review of the therapeutic uses of very-low-carbohydrate (ketogenic) diets. Eur J Clin Nutr 67: 789-796, 2013.
Ruskin DN and Masino SA: The nervous system and metabolic dysregulation: Emerging evidence converges on ketogenic diet therapy. Front Neurosci 6: 33, 2012.
Jansen, N., Walach, H.”The development of tumours under a ketogenic diet in association with the novel tumour marker TKTL1: A case series in general practice”. Oncology Letters 11.1 (2016): 584-592.
. Schwaab J, Horisberger K, Ströbel P, Bohn B, Gencer D, Kähler G, Kienle P, Post S, Wenz F, Hofmann WK, et al: Expression of Transketolase like gene 1 (TKTL1) predicts disease-free survival in patients with locally advanced rectal cancer receiving neoadjuvant chemoradiotherapy. BMC Cancer 11: 363, 2011.
Zhang S, Yang JH, Guo CK and Cai PC: Gene silencing of TKTL1 by RNAi inhibits cell proliferation in human hepatoma cells. Cancer Lett 253: 108-114, 2007
Multiple Sclerosis (MS) is a neurological disease caused by demyelination or breakdown of the myelin coating around the nerve cells (1). This is referred to as a neurodegeneration where the physical structure of the nerve is compromised, much like the coating around an electrical wire being chipped or stripped away. Common symptoms of MS are sensory symptoms in the extremities or face, unilateral visual loss, acute or subacute motor weakness of the muslces, diplopia (double vision), gait disturbance and balance problems, Lhermitte sign (electric shock-like sensations that run down the back and/or limbs upon flexion of the neck), vertigo, bladder problems, loss of control of a limb, and pain.
Initially, and for many years, the degeneration seen in multiple sclerosis (MS) was thought to occur because of an acute inflammatory attack on the cells by dis-regulated immune cells crossing the blood brain barrier. However, treatments focused on modulating the inflammatory attack seem to have no effect on the degeneration and demyelination. Thus, the actual definitive cause of this demyelination and neuro-degeneration has eluded us since 1868, when Jean-Martin Charcot first described it.
Recent studies point to evidence that this demyelation may be due to degeneration or breakdown of the nerve cell’s ability to use glucose as a primary fuel (2, 3). It is now theorized that MS may be due to a combination of degeneration and localized inflammation related to poor glucose uptake causing the demyelination which is seen in a number of MS cases (4, 5, 6).
A. Normal nerve cell with intact myelin sheath around the axon. B. Demyelinated axion nerve losing its ionic charge due to escape of potassium. C. Radio-labled tracer allowing visualization of demyelination on PET Scan
With this dual concept in mind, ketogenic diets have demonstrated some promising results when used with neurological diseases including MS. Ketogenic diets have been used in the treatment of epilepsy since 500 B.C. and in the treatment of obesity since 1860. It is now becoming apparent that ketogenic diets may play a very significant role in the treatment of neurological disease because of two-fold effects that arise when ketones become the primary fuel for the body.
First, when a person becomes keto-adapted and ketones are used as the primary fuel, instead of glucose, the body up-regulates mitochondria to use the ketones for fuel. As the ketone level rises, the need for glucose diminishes. This provides the nerve cell an alternative fuel source if glucose metabolism is impaired. It also decreases the need and production of insulin, a known hormone heavily involved in stimulating inflammation and inflammatory responses.
The second effect of a ketogenic diet is this favorable effect on inflammation. It has been demonstrated that a ketogenic diet decreases reactive oxygen species, increased production of superoxide dismutase and catalayse, all of which notably decrease the inflammatory effects of oxidative stress (9,10, 11). A ketogenic diet also is well known to raise glutithione levels, another anti-oxidant that decreases inflammation and oxidative stress (12-16). This same anti-inflammatory and keto-adaptation effect can be obtained from intermittent fasting.
To date, studies in patients with neurologic diseases like MS, Alzheimer’s disease using ketogenic diets have had positive results in memory, cognition and diminished inflammation with evidence of halting or reversing the chronic demyelination (17,18, 19). Still somewhat theoretical, the evidence points to effective dietary treatment and prevention for multiple sclerosis and other degenerative neurological diseases like Alzheimer’s Disease.
References:
J. M. Pearce, “Historical descriptions of multiple sclerosis,” European Neurology, vol. 1, no. 1, pp. 49–53, 2005.
C.-A. Castellano, S. Nugent, N. Paquet et al., “Lower brain 18F-fluorodeoxyglucose uptake but normal 11C-acetoacetate metabolism in mild Alzheimer’s disease dementia,” Journal of Alzheimer’s Disease, vol. 43, no. 4, pp. 1343–1353, 2014.
S. Nugent, S. Tremblay, K. W. Chen et al., “Brain glucose and acetoacetate metabolism: a comparison of young and older adults,” Neurobiology of Aging, vol. 35, no. 6, pp. 1386–1395, 2014.
H. Lassmann, W. Brück, and C. F. Lucchinetti, “The immunopathology of multiple sclerosis: an overview,” Brain Pathology, vol. 17, no. 2, pp. 210–218, 2007.
C. Confavreux and S. Vukusic, “Natural history of multiple sclerosis: a unifying concept,” Brain, vol. 129, no. 3, pp. 606–616, 2006.
P. K. Stys, G. W. Zamponi, J. van Minnen, and J. J. G. Geurts, “Will the real multiple sclerosis please stand up?” Nature Reviews Neuroscience, vol. 13, no. 7, pp. 507–514, 2012.
P. G. Nijland, I. Michailidou, M. E. Witte et al., “Cellular distribution of glucose and monocarboxylate transporters in human brain white matter and multiple sclerosis lesions,” Glia, vol. 62, no. 7, pp. 1125–1141, 2014.
L. C. Costantini, L. J. Barr, J. L. Vogel, and S. T. Henderson, “Hypometabolism as a therapeutic target in Alzheimer’s disease,” BMC Neuroscience, vol. 9, supplement 2, article S16, 2008.
P. G. Sullivan, J. E. Springer, E. D. Hall, and S. W. Scheff, “Mitochondrial uncoupling as a therapeutic target following neuronal injury,” Journal of Bioenergetics and Biomembranes, vol. 36, no. 4, pp. 353–356, 2004.
P. G. Sullivan, N. A. Rippy, K. Dorenbos, R. C. Concepcion, A. K. Agarwal, and J. M. Rho, “The ketogenic diet increases mitochondrial uncoupling protein levels and activity,” Annals of Neurology, vol. 55, no. 4, pp. 576–580, 2004.
T. Shimazu, M. D. Hirschey, J. Newman et al., “Suppression of oxidative stress by β-hydroxybutyrate, an endogenous histone deacetylase inhibitor,” Science, vol. 339, no. 6116, pp. 211–214, 2013.
S. G. Jarrett, J. B. Milder, L.-P. Liang, and M. Patel, “The ketogenic diet increases mitochondrial glutathione levels,” Journal of Neurochemistry, vol. 106, no. 3, pp. 1044–1051, 2008.
J. B. Milder, L.-P. Liang, and M. Patel, “Acute oxidative stress and systemic Nrf2 activation by the ketogenic diet,” Neurobiology of Disease, vol. 40, no. 1, pp. 238–244, 2010.
N. Dupuis, N. Curatolo, J. F. Benoist, and S. Auvin, “Ketogenic diet exhibits anti-inflammatory properties,” Epilepsia, vol. 56, no. 7, pp. e95–e98, 2015.
D. Y. Kim, J. Hao, R. Liu, G. Turner, F.-D. Shi, and J. M. Rho, “Inflammation-mediated memory dysfunction and effects of a ketogenic diet in a murine model of multiple sclerosis,” PLoS ONE, vol. 7, no. 5, Article ID e35476, 2012.
Y.-H. Youm, K. Y. Nguyen, R. W. Grant et al., “The ketone metabolite β-hydroxybutyrate blocks NLRP3 inflammasome—mediated inflammatory disease,” Nature Medicine, vol. 21, no. 3, pp. 263–269, 2015.
A. Ramm-Pettersen, K. O. Nakken, I. M. Skogseid et al., “Good outcome in patients with early dietary treatment of GLUT-1 deficiency syndrome: results from a retrospective Norwegian study,”Developmental Medicine and Child Neurology, vol. 55, no. 5, pp. 440–447, 2013.
Y. Ito, H. Oguni, S. Ito, M. Oguni, and M. Osawa, “A modified Atkins diet is promising as a treatment for glucose transporter type 1 deficiency syndrome,” Developmental Medicine and Child Neurology, vol. 53, no. 7, pp. 658–663, 2011.
M. Storoni and GT Plant, “The Therapeutic Potential of the Ketogenic Diet in Treating Progressive Multiple Sclerosis,” Multiple Sclerosis International, vol. 2015, Article ID 681289, 9 pages, 2015.
Join Dr. Nally on this evening’s Periscope as we talk about your biggest weight loss struggles in rapid fire style. We cover topics this evening from the effects of cheating on a ketogenic diet to how to overcome a weight loss stall . . . join us to hear the whole conversation.
Our very own, Jenna Lightfoot, PA-C, made it into the Cohost Contest Final Round for Jimmy Moore’s Low Carb Conversations. Listen to this intriguing review of the recent headlines and vote for your favorite candidate here.
At Nally Family Practice, where Jenna is one of our in-house Paleo/Low Carb experts, we thought that they all did a fantastic job. However, we’re a little preferential on who won this final round.
But, you should be the judge. So, click the link here, or down load the podcast from iTunes and make sure you vote ASAP!
KetoTalk with Jimmy & the Doc (the legendary podcaster Jimmy Moore from Livin’ La Vita Low Carb and his newest co-host, your’s truly, Dr. Adam Nally) makes its debut this Thursday, December 31st, 2015 on iTunes. You can see the show notes at KetoTalk.com (will be up and live on January 1st, 2016).
Throughout the exciting month of January, we will be airing a brand new episode of this 20-minute show each Thursday and a special bonus episode available on Sundays just to wet your ketogenic appetite and to kick off the podcast in its first month. Then, in February we’ll settle in to our regular Thursday time slot each week.
New podcasts can take a few days to assimilate into #iTunes, so don’t get discouraged if you don’t immediately see it up on iTunes. However, you can always find them at KetoTalk.com. Jimmy and I look forward to being your go-to, Ketogenic Lifestyle source for the latest and greatest in treating the diseases of civilization!
Get a sneak peek of our new show on tomorrow’s (Wednesday, December 30th) episode of “The Livin’ La Vida Low-Carb Show” where you can hear my interview with Jimmy as a preview what is sure to be a big hit in the #keto community. Thanks in advance for supporting our new podcast!
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:
the underlying cause. I see this problem in a very large majority of the people in my office and I am seeing people younger and younger show up with continually increasing blood pressure.
begin to back down their blood pressure medications, they would experience symptoms of dizziness, light-headedness, headache and a few patient’s nearly passing out. On a low-carbohydrate, high-fat (ketogenic) diet you need salt (sodium, potassium, & magnesium).
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).
