The health podcast legend, Jimmy Moore, and I talk about how much fat is too much. Or, is it? What’s the deal with Zero-carb ketogenic diets? We answer your questions and try to give you the most up-to-date knowlege regarding the ketogenic lifestyle and how it affects your metabolism. 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 we shoot them down one at a time.
You can down-load it for free on iTunesor listen to KetoTalk.com on your computer.
I’m sitting here at my home-office desk, on this beautifully hot 118° Arizona afternoon, eating this luscious piece of ketogenic Key-Lime & Blue-Berry Cheese Cake that my wife made for Father’s Day . . . pondering all the reasons ketosis has been a blessing in my life, specifically as a father. As I sit, reason after reason popped into my mind.
“Hmmm, I should share these . . . Why aren’t you sharing them?” I mused. So, with the the sweet tart of blue-berry on my palate and with a wipe of whipped cream from the corner of my lip, my fingers begin to click away on the keyboard.
What makes a person a father?
Testosterone –
Well, first, . . . Testosterone. I know. Leave it to a man to start with testosterone, but in the big picture, a man really isn’t a man if he doesn’t have a little extra testosterone, right? I mean, it was during the 5th week of embryonic development that my Y chromosome began signaling the differentiation of male fetal growth in-utero. And like every male, that same hormone testosterone continues to differentiate me from the human female counterpart throughout life.
Low testosterone has become a significant issue. 20-30% of the men in my practice suffer from some degree of suppression in testosterone when they first present in my office. In fact, you can’t watch late night TV any longer without being asked the question about low testosterone (Low ‘T’).
We know that the primary nutrient shown to affect testosterone to the greatest extent is fat. Studies reveal that diets low in fat are associated with lower testosterone compared to diets high in fat (1, 2). That begs the question, has 50 years of low fat diets made us less manly?
When did this become acceptable? And, does our diet of low fat have anything to do with it? I actually think it plays a role.
Testosterone is essential in providing energy, muscle mass & growth and actually keeping the waistline down. Adequate testosterone is one of the key components allowing the man to fill the father’s rolls of protector and provider, and if your diet doesn’t help stimulate its production, your less inclined to perform well in areas requiring its presence. That means that the bacon and eggs you crave in the morning lends toward your manliness, and the bagel and orange juice may be a little feminizing.
Fathers Need Muscles –
Second, father’s need muscles for all sorts of important things. It’s often Dad who carries the child on his shoulders, or lifts you above his head. It takes muscles for that.
We talked about the importance of testosterone in muscle development. That that’s not all. Many fathers can provide for their families specifically because of their ability to use that muscle. That’s not saying women can’t use muscle, too. I’m saying that a number of jobs that make our country function that require fitness, strength and muscle, like police, firefighters, construction, life-guards & delivery drivers. These jobs require muscle.
We now know that ketones, the primary fuel in a ketogenic diet, restrain muscle breakdown by decreasing leucine oxidation and preserving muscle mass (3). So, yes, visiting the donut shop actually does make you less manly by allowing the more rapid degradation of your muscles.
“Wasn’t it my muscles that first got your attention when we met and got this whole father thing started in the first place, honey?” I asked my wife in the kitchen.
“What?! No . . .” she responded.
“Oh, . . . never mind.”
Energy –
Whether you have great muscles or not, you need energy for the muscles you have to fill your role as a father. Work requires energy. As fat is increasingly used as fuel instead of sugar, the liver breaks it down and produces ketone bodies, or ketones. The liver itself, doesn’t use the ketones, so they are taken up by the muscles and brain for fuel. Increased energy, mental clarity and suppression of inflammation are the key findings that are noticed while using fat as your primary fuel. What father couldn’t us a little more of that?
In fact, several studies report that fathers have the biggest impact on the overall fitness and on the overall weight of their children. It was found that the father’s, not the mother’s, total and percentage body fat was the best predictor of whether or not the couple’s daughters gained weight as they got older (4). All the more reason to keep your waistline under control, Dad.
Another fascinating study showed fathers’ (again, not the mothers’) body mass index is directly related to a child’s activity level (5).
Energy and muscle is essential for “rough housing” and there is science to prove that “rough housing” makes your kids awesome! Psychologist Anthony Pellegrini, in the book The Art of Roughhousing, has found that the amount of roughhousing children engage in predicts their achievement in first grade better than their kindergarten test scores do. What is it about rough and tumble play that makes kids smarter? Well, a couple things.
Roughhousing makes your kids more resilient and resilience is a key in developing children’s intelligence. Resilient kids tend to see failure more as a challenge to overcome rather than an event that defines them. Intellectual resilience that comes from energetic fathers helps ensure your children bounce back from bad grades and gives them the grit to keep trying until they’ve mastered a topic.
Intelligence for You and Your Family –
Neuroscientists studying animal and human brains have found that bouts of rough-and-tumble play increase the brain’s level of a chemical called brain-derived neurotrophic factor (BDNF). BDNF helps increase neuron growth in the parts of the brain responsible for memory, logic, social intelligence and higher learning–skills necessary for academic success. We,also, now know that the brain that uses fat, or ketones, as it’s primary fuel recovers from injury and makes BDNF more effectively (6,7).
That rib-eye with steak butter your kids gave you for dinner is actually making you and them smarter and more resilient.
Overall Happiness –
The Harvard Grant Study completed in 1934, the longest longitudinal study ever done on the lives of men, found that a man’s father influenced his life in multiple ways exclusive to his relationship with his mother. Loving fathers imparted to their sons:
Enhanced capacity to play
Greater enjoyment of vacations
Increased likelihood of being able to use humor as a healthy coping mechanism
Better adjustment to, and contentment with, life after retirement
Less anxiety and fewer physical and mental symptoms under stress in young adulthood
It should be noted that “it was not the men with poor mothering but the ones with poor fathering who were significantly more likely to have poor marriages over their lifetimes.” Men who lacked a positive relationship with their fathers were also “much more likely to call themselves pessimists and to report having trouble letting others get close” (8).
You, as a father, matter. And, being in ketosis makes you an even better father! Seriously.
When all is said and done, a man’s relationship with his father very significantly predicted his overall life satisfaction at age 75 — “a variable not even suggestively associated with the maternal relationship” (8).
So, back to my key-lime blue-berry cheese cake, my wife just made me a better husband and father. Thanks, Dear!!
References:
Hamalainen, E., H. Aldercreutz, P. Puska, and P. Pietinen. Diet and serum sex hormones in healthy men. J. Steroid Biochem. 20:459-464, 1984.
Reed, M.J., R.W. Cheng, M. Simmonds, W. Richmond, and V.H.T. James. Dietary Lipids: an additional regulator of plasma levels of sex hormone binding globulin. J. Clin. Endocrin. Metab. 64:1083-1085, 1987.
Nair KS, Welle SL, Halliday D, Cambell RG. Effect of β-hydroxybutyrate on whole-body leucine kinetics and fractional mixed skeletal muscle protein synthesis in humans. J Clin Invest. 1988;82:198–205.
Figueroa-Colon R, Arani RB, Goran MI, Weinsier RL. Paternal body fat is a longitudinal predictor of changes in body fat in premenarcheal girls. Am J Clin Nutr. 2000 Mar;71(3):829-34.
Finn, Kevin et al. Factors associated with physical activity in preschool children. J of Ped., Vol 140, Issue 1, 81-85
Vizuete AF1, de Souza DF, Guerra MC, Batassini C, Dutra MF, Bernardi C, Costa AP, Gonçalves CA. Brain changes in BDNF and S100B induced by ketogenic diets in Wistar rats. Life Sci. 2013 May 20;92(17-19):923-8.
Masino SA, Rho JM. Mechanisms of Ketogenic Diet Action. Jasper’s Basic Mechanisms of the Epilepsies [Internet]. 4th edition. Bethesda (MD): National Center for Biotechnology Information (US); 2012.
Valliant GE. Triumphs of Excellence: The Men of the Harvard Grant Study. 1934
Does your diet really reverse vascular disease? I mean, will the diet you’re following ACTUALLY reverse the plaque burden that has occurred over the years of eating the SAD diet (Standard American Diet)?
It appears that the ketogenic diet does. At least that’s what research is showing, and that’s what I am seeing clinically. Let me give you an example. Reversal of vascular disease is what I saw last week in this patient case study in my office.
Meet “Mrs. Plaque” (name has been changed to protect her identity). She is a very pleasant 78 year old female who has been seeing me as a patient for the last 10 years. We identified worsening cholesterol and hyperinsulinemia in this patient a few years ago, and last year, she finally decided to go on a ketogenic diet after we noted slight worsening blood sugar (HbA1c increased to 6.1%), worsening cholesterol and a recent TIA (transient ischemic attack or “mini stroke”). We identified a 44% blockage in her left internal carotid artery and a 21% blockage in the right internal carotid artery putting her at risk for further cerebral ischemic events like a stroke and/or other vascular events like a possible heart attack down the road. She refused STATIN therapy as she had previous myalgia and side effects with their use in the past.
Past Medical History: Hyperlipidemia, Impaired Fasting Glucose (Pre-Diabetes),.Asthma, GERD, Irritable Bowel, Generalized Anxiety, Idiopathic Peripheral Neuropathy, Surgical Menopause (Hysterectomy) with Secondary Atrophic Vaginitis, Recent TIA, Cataracts, Appendectomy
Medications: Plavix 75mg one daily, Premarin Cream 0.635mg every other day, Xanax 0.5mg at bedtime for anxiety, Lyrica 50mg one nightly for neuropathy, Vitamin D 2000 IU daily , TUMS 750mg twice a day.
Her carotid ultrasound and carotid medial intimal thickness (CIMT) study completed April 1, 2015 is present below. You can see that her intimal thickness is only slightly higher than the average female her age, however, she has notable internal carotid artery blockage in both the right and the left sides.
The “mini stroke” and the report above, convinced her that she needed to tighten up her diet. The patient’s husband was also a diabetic and the patient had been “partially” restricting sugar in her diet up to this point in time, however, she had not fully jumped on the ketogenic band wagon. At this point she decided to change her diet.
She was placed on a ketogenic diet, restricting her carbohydrates to no more than 20 grams per day and increasing total fat to >50-60% of her total calories. Nothing else changed including her medications. She followed this program for the next year and this is the blood work that she had while following this program:
4/2/2015
8/4/2015
11/6/2015
5/12/2016
HbA1c (%)
6.1
5.8
5.2
Tot Chol (mg/dL)
224
156
230
233
HDL (mg/dL)
76
76
87
96
LDL-C (mg/dL)
134
65
128
123
Small Dense LDL-P (nmol/L)
481
150
222
217
Triglycerides (mg/dL)
72
76
74
68
Fasting Insulin (uIU/mL)
12
Glucose (mg/dL)
91
95
92
85
Because she was already partially restricting her sugar intake, her triglycerides and small dense LDL particle number was not bad, however, her average blood sugars were still significantly elevated. Weight decreased from 127 lbs to 119 lbs in August. She admits to slightly increased protein intake over the holidays and her weight increased back up to 125 lbs as of her last visit.
These labs also demonstrate that Total Cholesterol and LDL-C don’t appear to correlate with regression of plaque.
The image below is the patient’s repeat CIMT and carotid ultrasound 13 months later through the same lab. What is dramatic is that she has had over 10% regression in the plaque in both internal carotid arteries and a return of her carotid intimal thickness to the average female in her age bracket.
This case study is consistent with the findings of Dr.Shai and his group when they did a two year comparative dietary intervention study of Low Fat – Group 1, Mediterranean Diet – Group 2, and a Ketogenic Diet – Group 3 on vessel wall volume and CIMT.
Carotid IMT changed by −1.1% from 0.816 mm at baseline to 0.808 mm after 2 years (P=0.18), with no significant difference between diet groups (P=0.91). There was a trend toward significant correlation between the 2-year changes in carotid IMT and VWV (r=0.173, P=0.056).
So, does your diet reverse vascular disease? Evidence is pointing to the fact that the ketogenic diet does. I return to the statement Hippocrates made over 2000 years ago, “Let food be thy medicine, and let medicine be thy food.”
Ok, for those of you who are using Keto/OS (I commend you for your insightful use of the next step in ketogenic metabolism bio-hacking), I have discovered one of my new favorite mixes. (If you’ve already tried this mix, then where have you been and why didn’t you tell me about it?!)
Enter Keto//OS – exogenous ketones that aid in shifting you into ketosis. Yes, they actually do work and usually bump my ketones up 0.5 mmol/L to 1.5 mmol/L when I use them.
So, I mixed my orange flavored Keto//OS version 2.1 with Diet A&W Cream Soda, and voala, Orange Cream that takes me back to childhood memories!! You gotta try this.
As you know, I have no problem with using Diet Dr. Pepper, Diet Coke (NOT Coke Zero!), Diet Mug Rootbeer & Diet A&W Cream Soda. The sweetener that these four sodas use does not kick you out of ketosis, and I am OK with my patients using them on my Ketogenic diet. (Yes, I am OK with most of my patient’s using aspartame. Yes, I’ve actually read the studies . . . have you?! That’s why I’m OK with it’s use.)
If you haven’t tried Keto//OS yet, you can get your sample here.
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.
Listen in to Ketotalk Podcast #19 where we talk about inflammatory foods, building muscle with a ketogenic diet & how ketosis affects the Baby Boomer Generation.
Keto Talk is cohosted by 10-year veteran health podcaster and international bestselling author Jimmy Moore from “Livin’ La Vida Low-Carb” and Arizona Osteopath and Board 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.
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.
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.
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.)
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!
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.
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. . . .
It’s been cold this winter and as I was lighting a fire in the fireplace, a thought crossed my mind.
Why is it that only one match seems to start a forest fire, but it takes the whole box to start a campfire?
So, thinking back to my Boy Scout days, I began walking through the process of what it takes to get a good warm fire going. As a Boy Scout while camping in the snow, we used to have contests to see who could, using a single match, start the fastest camp fire. (We would use our most “MacGyver-like” skills). It occurred to me that the same timeless principles that allow one to ignite a fire with a single match are the same principles necessary for “fat burning.”
Maintaining ketosis is much like starting a campfire. There are some basic principles you need to understand. First, too much fuel keeps the fire from starting and too much carbohydrate or too much protein keeps the body from shifting into ketosis. Starting a campfire with a single match requires very fine thin strands of tinder to get started. If the peices are too big, the fire is smothered and cannot get started. It is the same with ketosis. Too much carbohydrate or protein smothers ketosis. You can get a copy of my ketogenic diet through registration on my membership site, by seeing me a patient face to face in the office or through a Tele-Medicine visit.
Second, oxygen is essential. For a fire to start, the flame needs a very small piece of fuel (wood or dryer lint) and large amounts of oxygen to burn. In ketosis, you have to provide the fat. If you’ve removed the carbohydrates and moderated the protein, but not provided enough fat to ignite the ketones, the body thinks it is starving, produces stress and shifts into making it’s own form of glucose for fuel through the process of glyconeogenesis (see my articles on why chicken salad makes you fat, and why your oatmeal is killing your libido).
Third, campfires often don’t have enough heat to get started. You have to get the temperature up before the wood can catch fire. This can be done in the camp fire by making a “cabin” the tinder can sit on and then building the “cabin” around the tinder as the fire builds and the heat increases. The increased heat and oxygen from under the tinder allows the larger pieces of wood to ignite and stay lit. In a ketogenic diet, the use of real food is similar to the cabin. Providing real food sources, instead of processed shakes and bars, allows for all the natural vitamins and minerals to let the ketosis start and ramp the metabolism up. Providing the correct vitamins also allows for the metabolism to have the ability to ramp up ketosis. I designed the KetoEssentials Vitamin specifically for this reason.
So, there you have it, the Paradoxical Effect of Fire and of Fat.
Don’t use too much fuel: Start with tinder for the fire – Limit the carbohydrates and moderate your protein (see how to balance protein here) to get into ketosis
Provide for increased oxygen for a fire – Provide adequate fat for ketosis
Provide a setting where the heat can build for a fire – Provide real food and appropriate vitamin sources for optimized metabolism in a ketogenic lifestyle.
You can see today’s Periscope discussion on this topic below:
On this evenings PeriScope video we talked about cholesterol. And, and you can see an updated, in depth discussion about cholesterol on my YouTube channel here. Please go check it out and if you find it helpful, please follow me here and on YouTube. The is the burning question on everyone’s mind who starts a Low-Carb, High Fat or Ketogenic Diet: “What will happen to my cholesterol if I lower my carbohydrates and eat more fat?”
The answer . . . it will improve!
How do I know this? I’m an obesity specialist. I specialize in FAT or lipids (to put it kinder scientific terms). To specialize in fat, one must know where it came from, what it’s made of and where it is going. And, this has been the case with every single patient I have used this dietary change with for the last ten years, myself included.
Lets start with the contents of the standard cholesterol or “Lipid Panel”:
Total Cholesterol
HDL-C (the calculated number for “good” cholesterol)
LDL-C (the calculated number for “bad” cholesterol).
Triglycerides
The first problem with this panel is that it makes you believe that there are four different forms of cholesterol. NOT TRUE! Actually cholesterol is cholesterol, but it comes in different sizes based on what it’s function is at that moment in time. Think of cholesterol as a bus. There are bigger busses and smaller busses. Second, triglyceride is actually the passenger inside the HDL and the LDL busses. And third, Total Cholesterol is the sum of the HDL, LDL, as well as ILDL & VLDL which aren’t reported in the “Lipid Panel” above.
The fourth thing that this panel doesn’t tell you is that HDL & LDL are actually made up of sub-types or sub-particles and are further differentiated by weight and size.
For our conversation, we need to know that the number of LDL particles (LDL-P) can actually be measured in four different ways and these measurements have identifed that there are three sub-types: “Big fluffy” large dense LDL, medium dense LDL, and small-dense LDL. Research has identified that increased numbers of small-dense LDL correlates closely with risk for inflammation, heart disease and vascular disease (1).
If you’ve been a follower of my blog for a while, you’ve seen this picture before. This picture illustrates why an LDL-C (the bad cholesterol measurement) can be misleading. Both sides of the scale reflect an LDL-C of 130 mg./dl. However, the LEFT side is made up of only a few large fluffy LDL particles (this is the person with reduced risk for heart disease) called Pattern A or a LDL healthy cholesterol level. Even though the LDL-C is elevate above the recommended level of 100 mg/dl, the patient on the left has much less risk for vascular disease (this is why you CAN’T trust LDL-C as a risk factor).
The RIGHT side of the scale shows that the same 130 mg/dl of LDL-C is made up of man more small dense LDL particles (called “sd LDL-P”) with a Pattern B type that is as increased risk for heart or vascular disease. This is where the standard Lipid Panel above, fails to identify heart disease and it’s progression.
Research tells us that the small dense LDL particle levels increase as the triglycerides increase. And we know that Triglyceride levels increase in the presence of higher levels of insulin leading to a cascade of inflammatory changes. Insulin is directly increased by the ingestion of simple and complex carbohydrates. Insulin also increases with the ingestion of too much protein. So, that chicken salad or the oatmeal you ate, thinking it was good for you, actually just raised your cholesterol. If you are insulin resistant, your cholesterol just increased by 2-10 times the normal level (see my article here on how insulin resistance causes this.)
“Ok, but Dr. Nally, there are four different companies out in the market measuring these fractional forms of cholesterol. Which one should I choose?”
There are actually five different ways you can check your risk.
Apolipoprotein levels. This can be done through most labs; however, this test doesn’t give you additional information on insulin resistance that the other tests can.
Berkley Heart Lab’s Gradient Gel Electrophoresis – This test gives a differentiation based on particle estimation between Pattern A and Pattern B
Vertical Auto Profile (VAP-II) test by Arthrotec – This test determines predominant LDL size but does not give a quantifiable lipoprotein particle number which I find very useful in monitoring progression of insulin resistance and inflammation.
NMR Spectroscopy from LipoScience – This test measures actual lipoprotein particle number as well as insulin resistance scores and will add the Lp(a) if requested. I find the NMR to be the most user friendly test and useful clinically in monitoring cholesterol, vascular risk, insulin resistance progression and control of the inflammation caused by diabetes. This test has the least variation based on collection methods if frozen storage is used.
Ion-Mobility from Quest – This test also measures lipoprotein particle number but does not include insulin resistance risk or scoring. Because the test is done through a gas-phase electric differential, the reference ranges for normal are slightly different from the NMR.
In regards to screening for cardiovascular risk, the use of all five approaches are more effective than the standard lipid panel. However, I have found that clinically the NMR Lipo-profile or the Cardio I-Q Ion-Mobility tests are the most useful in additionally monitoring insulin resistance, inflammation, and disease progression.
It is was the use of these tests that demonstrated to me the profound effect of carbohydrate restriction and ketogenic lifestyles on vascular and metabolic risk. We talk more about these tests on my YouTube video .
Hope this helps.
References:
Williams PT, et al. Comparison of four methods of analysis of lipoprotein particle subfractions for their association with angiographic progression of coronary artery disease. Atherosclerosis. 2014 April; 233(2): 713-720.
Ketogenic Lifestyle Rule #2: Life Begins at the Edge of Your Comfort Zone
We have been taught for over 50 years that the minimum carbohydrate intake necessary to maintain health is 130 grams per day, with the average diet of 2000 calories per day containing around 300 grams per day based on 1977 recommendations that 55-60% of are dietary intake should come from carbohydrates. This value was initially established during World War II by a committee of scientists tasked with determining dietary changes that might effect national defense (1). These “guidelines,” originally called the Recommended Daily Allowances (RDA) and accepted by many as the gospel truth, have been modified every ten years and in 1997 changed to the Dietary Reference Intake (DRI). However, the recommended carbohydrate values have not changed other than “avoiding added sugars” in the most recent 2015 recommendations.
In light of the fact that there are NO actual diseases caused by lack of carbohydrate intake, most dietitians and physicians still preach the carbohydrate dogma originally outlined by the RDA. I say dogma, because these recommendations are based on a diet that vilifies fat, particularly animal fat like red meat. Say the words “red meat” around a dietician these days you’d think Voldemort (“He Who Shall Not Be Named”) had returned.
I bring up the carbohydrate quandary because it is a question that I am asked every single day. The question that seems to be asked of me, more and more, is what exactly is a carbohydrate?
Let’s make it simple. There are really only three types of carbohydrates:
Sugar
Starch (known as complex carbohydrates)
Fiber
Let’s start with Sugar. The simple form of carbohydrates, and the form that spikes your blood sugar and insulin rapidly, are called mono-saccharides (glucose, galactose, fructose & xylose). When two of these mono-saccharides are bound together they form disaccharides like sucrose, also known as “table sugar” (glucose + fructose), lactose found in milk (glucose + galactose), and maltose found in cereals and sweet potatoes (glucose + glucose).
Milk Sugar or Lactose (glucose + glucose)
The simple monosaccharides or disaccharides are easy broken into their mono-saccharide form in the blood stream and require the body to produce insulin to be used. The person with insulin resistance, impaired fasting glucose or type II diabetes often produces 2-10 times the normal amount of insulin to correctly use these mono-saccharides (see why this is a problem in: The Dreaded Seven: Seven Detrimental Things Caused By High Insulin Levels). Remember, fruit is also simple sugar containing the mono-saccharide fructose . . . which we call “natures candy” in my office.
“Yea, I know sugar is bad for me, but Dr. Nally, I just eat the good starches.”
If I had a nickel for every time I’ve herd that phrase . . .
We’ve become comfortable with shunning fat and “simple sugar,” but in the process we’ve been eating more “good starch.” But the “good starches” are also saccharides – just in longer chains of more than three glucose molecules bound together. Our gut easily breaks the bonds between the glucose links and turns these starches into mono-saccharides to be used as fuel. It takes a bit longer than the simple sugars above, so the release of insulin is slower (which is why it has a better glycemic index score), but whether you produce the insulin in the first hour or the second hour after eating it, insulin is still insulin. In the case of insulin resistance, the damage is still done.
These good starches make up “comfort food” like bread, rice, pasta, potatoes, corn, grains & oats. To the patient with insulin resistance, impaired fasting glucose or type II diabetes, the higher insulin response stimulates increased weight gain, rise in cholesterol, shift in hormone function and progression of atherosclerosis (vascular and heart disease). See the recent article on Why Your Oatmeal is Killing Your Libedo.
What about “resistance starches?” These are still starches and I am finding clinically that they still cause a rise in insulin and push people out of ketosis (See Common Ketosis Killers).
Finally, Fiber. Fiber is a carbohydrate, however, it is the indigestible part of the plant. Fiber has double bonds between the saccharides that human gastrointestinal tracts cannot digest. In most cases, fiber passes right through the intestines without being digested. It actually acts like a broom for your colon, helping the intestines to move nutrients through the system. This is why I recommend 1-2 leafy green salads a day for most patient’s following ketogenic diet. Fiber does help to promote bowel function.
The Leafy Greens
Fruit, non-green vegetables, pasta, grains and breads do contain good sources of fiber, however, these foods also have absorbable starches making them problematic as noted above.
The take home message is this, the use of starch or simple carbohydrate will be problematic for weight loss, cholesterol control, blood sugar control or blood pressure control in a patient with insulin resistance.
Therefore, the ketogenic lifestyle truly begins at the end of your comfort zone.
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.
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
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!
It’s Here! KetoTalk with Jimmy Moore and the Doc premiers today. You can link to it here: http://ketotalk.com/2015/12/0-keto-talk-with-jimmy-moore-the-doc-debuts/ or click on the menu bar above to take you to KetoTalk.com.
The show has been picked up by iTunes, but it takes anywhere from 3-7 days to appear in their search menus, so be patient and while iTunes assimilates it, you can always hear it or download it from KetoTalk.com.
We want to hear your feed back so please tell us what you think and rate us on iTunes when it is available.
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’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.
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).