Salt #DocMuscles #KetonianKing

What If Salt Actually Improves Blood Pressure & Blood Sugar?

What if increasing your salt intake actually improved your diabetic blood sugar?

What if increasing salt intake actually lowered your blood pressure?  Could it be that easy?

Just about every patient that I see has significant worry about salt intake.  Some greater than others. In fact, some people are so salt phobic that when I encouraged its use, they called me a “quack” and left my practice.  But does salt restriction really work, or is it doing more damage than we think?

That was the question that was asked by Dr. Ames in the American Journal of Hypertension 17 years ago.  However, his answer never got a mention.  In fact, I’ve been in practice for almost 18 years, and incidentally stumbled upon this article when it was mentioned by a colleague of mine.   Granted, it is a small sample of people, only 21 in the study.  However, the results are profound.

21 patients with hypertension were randomized to periods of no salt (placebo) and periods of 2 grams (2000 mg) of sodium chloride four times a day (a total of 8 grams of salt per day).  Glucose tolerance tests were completed with insulin levels at the end of each intervention period.

Insulin Resistance and Hypertension Improve by Adding Salt

What was noteworthy was that those with insulin resistance and diabetes had improvement in their glucose levels while on sodium supplementation.  Those with hypertension had improvement in their blood pressure while on the sodium supplementation.   Lastly, those with insulin resistance had a lowering of their insulin levels during the period of increased sodium intake.  These findings fly in the face of the dogma that’s been drilled into our heads that “salt is bad!”

“But, you can’t base your findings on a small group of 21 people,” the experts say.

Yes, it is a small study group. However, these findings are what I, also, have seen clinically in my practice for over 13 years.

We know that the average human needs 3 grams of sodium per day and 3 grams of potassium per day.  If you’re eating the standard American diet (SAD diet) including processed foods, you’re getting 2-3 grams per day of sodium.  In fact, the CDC claims the worst meals for you are:

  • Bread
  • Processed chicken dinners
  • Pizza
  • Pasta

However, if your following a low-carbohydrate or ketogenic lifestyle, you won’t be eating the meals above and you’re probably not getting near enough salt.  This is the cause of the keto-flu I wrote about a few weeks ago.  And, according to the study above, it is a potential driver of our persisting insulin resistance, diabetes and hypertension.

How Much Salt Should I Use?

In my office, I encourage use of 3-4 grams of sodium and 3-4 grams of potassium daily when using a ketogenic lifestyle.  That’s approximately 1 1/2 – 2 teaspoons of salt per day.  I like the Himalayan Pink Salt because it contains sodium, potassium, magnesium and zinc.

Could it be that salt restrictions are making our insulin resistance and blood pressure worse?  That’s what the clinical evidences are pointing toward. However, more research is still needed.

Want to know more about a ketogenic life-style?  Click the link on KetoLife above to get some basics.  If you’re already following a ketogenic lifestyle, then let me help you navigate the bumps and turns by going to the KetoKart and checking out the products I recommend to jump-start ketosis DocMuscles style!

Until then, I’ll have another piece of bacon, please . . . and, oh, pass the salt!

The Keto-Flu

So, you have the keto-flu.  No, you’re not contagious.  No, you can’t pass it on to someone else, or catch it when your friend who follows a ketogenic lifestyle sneezes.

Actually, congratulations are in order. You’ve just experienced the amazing metabolic shift that jump-starts the healing process in your body.  You’re shifting to a metabolism that optimizes the use of fat in the form of ketones.  During this transition, usually within the first week, people can experience a series of symptoms that have been dubbed the “keto-flu.”


What are the common symptoms of the keto-flu?

  • Fatigue
  • Headache
  • Brain Fog
  • Dizziness
  • Nausea
  • Irritability
  • Light-Headedness
  • Leg Cramps

These symptoms can last 3-5 days, in some people I’ve seen it last as long as two weeks.   But, if you weren’t expecting it, and you don’t know what it is, it can be kind of discouraging.  Don’t despair, however, if you know what it is, you can usually do a couple simple things to prevent it, or at least cause the symptoms to dramatically improve.


The keto-flu is usually caused by a shift in your body’s use of water and salt. Insulin causes the kidneys to retain sodium. When you change to a ketogenic lifestyle, your insulin levels fall to baseline and your body is able to use the sodium and potassium to remove the excess water production in each cell from fat burning. (If it didn’t, you’d swell up like beached whale.) This isn’t a bad thing, it just means that you need to add these electrolytes back into your diet in a greater degree.

The average adult human needs 3-4 grams of sodium each day and 3-4 grams of potassium each day to balance out water use and make all the cells happy.  So, what’cha wait’n for? Make your cells happy.

How To Treat It

I find that putting 1/2 teaspoon of salt (I like the Himalayan Pink sea salt because it contains sodium, potassium, magnesium and zinc) in a glass of water cures the symptoms very rapidly, sometimes within minutes. It’s amazing how fast you suddenly feel the brain fog lift and your energy returns.

Another option is using a bouillon or bone broth with your meal. This adds to the overall enjoyment of the meal and replaces these needed electrolytes in a very tasty way.

If the salt replacement doesn’t do the trick, then your keto-flu may be related to the need for more fat. Often, people who start a ketogenic lifestyle cut out the carbs, but don’t put enough fat back into the system.

On the traditional American (or insert your own country of residence here) diet the body uses carbohydrate as its primary fuel and protein for building blocks. When you cut out the carbs, your body will continue to use the protein for building muscle, skin and connective tissue. However, if you don’t give it enough fat to replace the carbohydrate you removed, it’s like running your car on fumes.

You’re body will run for a while, but not very well.  And, in some cases, you’ll feel like you were left on the side of the road with a body that doesn’t want to go anywhere.  You’ll feel like the gas tank is empty.

If you’re not used to a diet higher in fat, your body also has to “fat-adapt,” sometimes called keto-adaptation.  This is the process of your gut and cells up-regulating MCT receptors (fat channels or doorways for fat) to enter more efficiently.  This can take a few weeks, and for some a few months.  Not giving yourself enough fat in a ketogenic lifestyle can slow this adaptation process and also give you keto-flu-like symptoms.

What If It Doesn’t Improve?

If the leg cramps haven’t improved with the replacement of the salts and fat, you might consider yellow mustard.  Mustard contains sinapoline that when metabolized through the acid of the stomach in the body has a byproduct that is similar effect to that of quinine.   Patients, and myself included find that dipping summer sausage or your favorite hard cheese in some yellow mustard before bed does wonders in prevention of muscle cramps or spasm.

If the nausea turns to vomiting, or if the headache or fatigue worsens with added weakness, then it’s time to call your doctor and get checked out.  Vomiting, weakness and worsening fatigue are signs of something more serious.  If this happens, call your doctor.

What About Exogenous Ketones?

Lastly, the addition of exogenous ketones (ketones bonded to a salt) are also very helpful in this transition period.  Drinking exogenous ketones provides added ketones, rapidly absorbed into the blood stream, and second they provide some of the sodium, potassium or magnesium needed as a replacement.  You can check out my Ketogenic Kick-Start packages here.  Or, you can go to Dr. Nally’s favorite ketone store at and order them directly.

Either way, I hope you find this helpful as you transition to your Ketogenic Lifestyle.

Smoked New Year’s Eve Ribeye Roast

I’ve been admiring rib-eye roasts over the years.  I also love the prime rib from which they are made.  It has been a secret desire of mine to  be able to make my own keto friendly smoked rib-eye roast or prime rib, and when I was in Costco last week, I saw a beautiful roast on sale.  Over the last 12-13 years of following a ketogenic life-style, I’ve developed a palate for a good rib-eye or prime rib cut cooked to perfection.

So, what does a man do when shown meat on sale, and his wife is no where to be found?

Yep, you guessed it. . . I’m now the proud owner of a beautiful rib-eye roast.

After much perusing of the various “inter-webby” recipes and smoker recommendations, this is what I came up with.

Out of the package, you can see this marvelous bone-in roast is delightful. (Actually, this is the picture is of the 20 lb roast from the Costco website.)  Mine only had four bones and was only 5 lbs, but as a male, when you see this picture, you have to wipe the drool off the corners of your mouth.

I peeled back the excess fat from the meat side and then, I trimmed up the excess fat off the bone for presentation.

Dr. Nally’s Butter Herb Butt Rub

I then created the following butter/herb rub:

  • 1 cube of butter
  • 2 tablespoons freshly chopped sage
  • 2 tablespoons freshly chopped time
  • 2 tablespoons freshly chopped rosemarie
  • 1 tablespoon parsley flakes
  • 10 garlic cloves dices

This is a good time to fire up your smoker or go out and ignite your pellet smoker.


I use a Traeger Select Elite pellet smoker

For the busy doc, this works nicely for me, and it works as that best grill I’ve ever used as well (but, that’s for another post).  I like this because you can purchase various pellet types based on the meat you’re smoking.  For a number of my steaks, I like to use the mesquite pellets, however, I picked hickory for this roast.  You could use oak or even cherry might be nice.  Traeger sells a mixture of woods for those days when you really can’t decide. 

For this roast, you want to get your smoker going and up to 275 degrees.

Once my smoker was heated up and set to my desired temperature, I went back into the kitchen and I finished up my rub.  The butter was softened for 20 seconds in the microwave and the herbs were all added to the butter and mixed nicely.


Prepping the Roast

A slice in the rib-eye roast was made every two inches parallel with the bones on top and bottom, and the butter/herb mixture was rubbed onto all sides of the roast, making sure to stuff the incisions in the meat with extra butter/herb mix. Then, my favorite rub was patted liberally all over the roast. The butter gives a nice adhesive for my liberal application of the butt rub of choice.

I’m a huge fan of Bad Byron’s Butt Rub Barbecue Seasoning. It is keto-friendly, one of the few that doesn’t have added sugar, maltodextrin or dextrose that I’ve found (unless you make your own). See my article on sweeteners if you are wondering why this is important.

Smoker prepped . . . check!

Keto friendly smoked rib-eye roast prepped . . . check!

Roast has been rubbed down . . . check!

We’re ready!

The roast was placed on the smoker/grill and timer was set for 2 hours. This will put your internal temperature somewhere between 125-135 degrees. I like my rib-eye medium, so I may need to leave it on for an hour longer.

Meat Preparation Temperatures

Unfortunately, no one ever explains this stuff to you, so, I found a nice temperature chart on the (thanks G. Stephen Jones!)  The goal for the meat is to get it to the temperature below when it is served.  If the meat is pulled off the smoker around 5 degrees below the temperature listed below, and you give the meat 5-10 minutes to “rest” while covered with some foil, the bone will bring the core temperature to the desired preparation temperature.  I’ve modified the list below for my and your easy viewing pleasure here:


Medium-Rare Medium


Beef Steaks


135° 145°


Beef Roasts

125° 130° 145°


Lamb Chop


135° 145°


Lamb Roast


130° 145°


Pork Roast




Veal Chops




Veal Roasts




Adapted from

Note: These are NOT USDA recommendations.  The USDA temperatures are notably 10-15° higher because of food safety issues, however, many professional chefs are not cooking your medium-rare steak to 150°.  You’d send it back in a heartbeat if that were the case.

Next, the cooking process begins.  With the smoker pre-heated to 275 degrees, the roast was placed on the smoker, bone side down.  I closed the lid . . . and began writing this post.

At the two hour mark, the roast was up to 120 degrees with my old meat thermometer.  My next investment will be an instant read digital Thermopro meat thermometer that gives an instantaneous and accurate core temperature of your roast.  After cooking this roast, I can see why one would be very helpful.

It actually took 3 hours to reach a core temperature of 140 degrees.  It was worth the wait.  My wife and daughter are not usally fans of prime rib or rib roast in the past, however, they devoured this.  I don’t think I will ever order prime rib again, when I can cook my own that tastes this good.

Why post something like this?

First, smoking meat makes you feel like a man.  Seriously, your testosterone feels like it goes up by 50-100 points smoking a good slab of meat.  People always ask me what I personally eat on holidays or celebrations.  This is a do-able recipe you can add to your file, and your man card.

Second, the preparation for this took me no more than 15 minutes, and I chopped and diced all my own fresh herbs.  It would have taken me 3 minutes to do this if I hadn’t used fresh herbs.

Third, This roast cost me $45 at Costco and it will serve eight to ten people (or my family and lots of really yummy left overs for the next week).  And, each steak I slice off this roast tastes like I took my family for $60 a-piece steaks at the fancy over-priced steak house down the road . . . I call it “gourmet-keto for the budget conscious.”

Anyway, leave me your comments. And, if you have a favorite smoker recipe.  Include Bacon Boy (you can find his printable image in the right side panel) in the picture, and I’ll enter you in a drawing for the next Keto-Cart Kickoff.

Happy New Year!!


#CholesterolInKetosis #DocMuscles #KetonianKing #Cholesterol #LDL-C

The Ketogenic Cholesterol Quandry

“Won’t my cholesterol get worse and increase my risk of heart disease if I eat more fat?”

I get asked this question at least 3-4 times a day.  The answer is, “NO. Not if you cut out the sugar and starch.”

“But, wait?! What about my heart?  All that fat can’t be good for my heart?” they ask.

Cholesterol Defined

Let’s start with the contents of the standard cholesterol panel or “Lipid Panel.”

For the last 20-30 years the following labs have been looked at as the holy grail of heart disease risk:

  • Total Cholesterol
  • HDL (the measured number for “good” cholesterol)
  • LDL-C (the calculated number for “bad” cholesterol).
  • VLDL-C (the calculated number for very low density 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 a steroid precursor that either makes up a part of the lipoprotein molecule or is transported with the triglycerides as a passenger.   The lipoproteins are just transporters made of lipid that are only slightly different from their passenger load (causing increased or decreased density).  The proteins that are contained within the wall of the lipoprotein transporter is what makes them different.  These lipoprotein particles can be thought of, simplistically as buses, carrying triglyceride passengers.  Here size does matter, and size determines the function of the molecule at that moment in time.

Cholesterol is Really Just a Triglyceride Bus

These buses, big and small, carry the passengers up and down the vascular system of the body.  Glucose can float freely through the blood stream, but the other form of fuel, triglyceride, must be transported via the “lipoprotein bus”.  The triglyceride and cholesterol are actually the passengers inside the bus.   But triglyceride presence in the system seems to change the density of the lipoproteins.  So now picture big, medium and small buses . . . the high density lipoprotein (HDL), intermediate density lipoprotein (IDL) and the low density lipoprotein (LDL) buses.

#Choleserol #Ketosis #KetonianKing #DocMuscles

Triglyceride Changes the Density of Cholesterol

The density of the bus gets lower as triglyceride levels rise and fewer cholesterol esters and proteins are bound.  As HDL goes up, LDL-C goes down (Parker TS et al, Proc Natl Acad Sci USA, Feb 1986)

The second problem is the VLDL-C and LDL-C are actually calculated numbers and don’t actually reflect the true presence of the lipoprotein particles as the triglyceride number rises. For the accountants, mathematicians and engineers reading this that calculation is called the Friedwald Equation and is as follows:

  • LDL-C mmol/L = [Tot Cholesterol (mmol/L)] – [HDL-C (mmol/L)] – [TG (mmol/L) / 2.2]
  • LDL-C mg/dL = [Tot Cholesterol (mg/dL)] – [HDL-C (mg/dL)] – [TG (mg/dL) / 5]
  • VLDL-C = [TG / 5] as a calculated estimate
    • This equation falls apart when the triglyceride level is greater than 400 mg/dL (4.52 mmol/L) or patients with hyperinsulinemia.

Total Cholesterol is the sum of the HDL, LDL, as well as intermediate density lipoprotein (IDL) & very low density lipoprotein (VLDL) which aren’t reported in the “Lipid Panel” above.  So, total cholesterol is basically the sum of all the buses you have driving around.

The third key piece of information that the Lipid Panel above doesn’t tell you is the lipoprotein categories (HDL, LDL, IDL, and VLDL) are actually have three to four sub-types or sub-particles that are further differentiated by weight and size.

#DocMuscles #KetonianKing #BerkleyHeartLabs #CholesterolSubParticles
Image Credit: Berkley Heart Labs, Inc.

Improvement in cardiovascular risk, including improvement in cholesterol, inflammation and plaque formation have been the case with every patient I have used a high fat, low carbohydrate (ketogenic) dietary approach with over the last 12 years.

I’ve had so many people ask me how this works, and then, how to explain the changes to their primary doctors or cardiologist, I decided to write the following article.  My intent is not to point the finger where others are wrong; but to identify how we, myself included, took a misstep along the path of scientific discovery.  This misstep led to guidelines that, for over 45 years, have been accepted by medical students and clinicians as the “gospel truth.”

History of Cholesterol Measurement

The measurement of cholesterol, specifically total cholesterol, started in the 1950’s. There appeared to be a mild correlation of heart disease in countries who’s diets had higher fat intake. Ansel Key’s identified this apparent correlation in his Diet-Heart Hypothesis published in JAMA in 1957.  He stated from his observational work that “the results of a fatty diet are hypercholesterolemia [elevated cholesterol].” A number of studies at the time showed that increasing fat intake in the standard diet increased total cholesterol; however, NO LINK to heart disease was ever proven (Ahrens EH, Jr, Lancet, May 1985).

Studies published by E. H. Ahrens, Jr.  demonstrated that the cholesterol increased because of carbohydrate intake, not fat alone (Ahrens EH Jr, et al., Trans Assoc Am Physicians, 1961).  The actual question, “Does increasing fat alone cause heart disease?” was never answered. The question, as well as known evidence based cholesterol reducing dietary approaches, were ignored in 1984 by the National Institutes of Health (NIH) Consensus Development Conference on Lowering Cholesterol to Prevent Heart Disease that was based heavily on epidemiological data rather than clinical reproducible science (Ahrens EH, Jr, Lancet May 1985).

Despite significant scientific evidence refuting the Diet-Heart Hypothesis, the 1984 NIH decision reflected politics and massive publicity campaigns.

Stop Demonizing My Eggs!

Since 1984, fat and cholesterol containing foods are treated like witches of Salem.  As an example, eggs, specifically the egg yolk.  (To this day, the chef at every breakfast bar I’ve ever visited asks if I want an egg white only omelet.)  Interestingly, there is actually no scientific data association between whole egg consumption and heart disease.  The science simply does not exist. Seriously, check for yourself.

#BaconEggs #DocMuscles #KetonianKing

You can’t extrapolate mortality risk based on a single small study that doesn’t actually identify correlation or causation.  But the AHA did exactly that in 1961, and they are trying to do it again today.   The MR-FIT study, largest study ever completed, is incessantly quoted as the study that demonstrates reduction in cholesterol leads to reduction in cardiovascular disease, but this trial was actually a failure and did not demonstrate improved risk by lowering cholesterol.  In fact, the Director of the study, Dr. William Castelli actually stated, “. . . the more saturated fat one ate, the more cholesterol one ate, the more calories one ate, the lower people’s serum cholesterol…”

“We found that the people who ate the most cholesterol, ate the most saturated fat, ate the most calories weighed the least, and were the most physically active,” he said.

Diet-Heart Hypothesis Doesn’t Explain the French Paradox

To add to cholesterol confusion, the Diet-Heart Hypothesis does not explain the “European or French Paradox.”  The French prefer cooking in butter instead of vegetable oil.  In fact, the French eat 40% fat in their diet. And, more than 15% of that is saturated fat.

#FrenchParadox #DocMuscles #KetonianKing
The French Paradox

Interestingly, the French and those that eat the most cheese, butter and whole eggs have the lowest rate of coronary vessel calcification and heart disease.  Attempts to explain this away as epidemiological error or diet complexities have been published, but still never answers the underlying question, “Does increasing fat alone cause heart disease?” (Ferrieres J, Heart, Jan 2004).

According to the Diet-Heart Hypothesis, people with familial hypercholesterolemia should have much shorter lifespans and are at increased risk of early mortality or death.  However, there is actually no scientific evidence of this.  In fact, the Honolulu Heart Program study revealed that people with low cholesterol are the ones at significant risk of early mortality or death (Schwartz I, et al., Lancet 2001 Aug). Additionally, higher LDL-C is actually predictive of longer life and has been demonstrated to correlate with longevity (Ravnskov U et al., BMJ Open, 2016 Jun 12;6(6): e010401).

Saturated Fat Isn’t Bad

I hate to burst your bubble, but saturated fat is NOT linked to vascular disease, diabetes or increased mortality (de Souza RJ et al., BMJ 2015,351:h3978).

It is commonly understood that LDL-C will rise as you eat more saturated fat.  This is normal on a ketogenic diet. It has been reported in the scientific literature for over twenty years. It is to be expected, because LDL-C is really a measurement of three different LDL sub-particles (“big fluffy, medium, and small dense”).  Increased saturated fat intake, while at the same time lowering carbohydrate intake, actually causes a shift in these low density particles to a bigger “fluffier” particle conformation (Griffin BA et al., Clin Sci (Lond), 1999 Sep).  We know that the small dense LDL particles are the atherogenic / inflammatory particles participating in the formation of vascular disease and directly correlate with triglyceride levels. We also know the big “fluffy” LDL particles actually reduce the risk of vascular disease  (Griffin BA et al., Clin Sci (Lond), 1999 Sep).

#CholesterolParticleSize #KetonianKing #DocMuscles

Why Do Physicians Still Prescribe STATIN Medications?

So why have clinicians been pushing the use of STATIN medications to reduce risk of coronary heart disease?  It started with the Lipid Research Clinics Coronary Primary Prevention Trial (LRC-CPPT).  This was a study of over 3800 men treated with cholestyramine, a cholesterol lowering medication (JAMA, 1984 Jan. 20;251(3):351-64.).  There was a very slight “absolute reduction” in coronary heart disease risk, 1.6% to be exact.  LDL-C decreased, but there was no reduction in the risk of death.   In fact, there was actually an increase in risk of all cause mortality in the cholestyramine group which was never emphasized.

Overall, cholestyramine reduced non-fatal heart attacks in 60 of the 3,806 men.  In other words, one in 63 men improved with the use of this medication . . . not very impressive.  However, statistics look more impressive expressed in terms of “relative risk.”  Relative risk is the percent increase of those with no treatment from those with treatment.  This is always a bigger number.

When the LRC-CPPT researchers calculated relative risk, the percent change between the treated and non-treated was 19%.  This bigger number was reported as the “risk reduction.”  For those that don’t know the difference between actual risk and relative risk, 19% sounds very impressive! (JAMA. 1984 Jan 20;251(3):351-64.)

False Evidence Emphasized By Relative Risk

This relative risk reduction drove the STATIN era we are well aware of today.  Lipitor (atorvastatin) reduces heart disease risk by only 1%.  However, when you use the term “relative risk reduction,” it has more psychological effect. Relative risk of 36% sells more drugs.

Crestor (rosuvastatin) was show to have an absolute risk reduction in heart disease by 1.2%.  When run through the relative risk reduction statistic it has a claim of 44% relative risk reduction.

These big numbers emphasized false evidences in many clinician’s minds that reducing LDL-C must be really effectively reducing heart disease.

Knowing that the LDL-C doesn’t really give you a clear idea of heart disease risk.  It becomes essential to know which type of LDL lipoprotein particle is the atherogenic or heart disease causing particle. Research now points to the small-dense LDL particle as the atherogenic molecule (Hoogeveen RC et al., Arterioscler Thoromb Vasc Biol, 2014 May; Ivanova EA et al., Oxidative Med Cell Longevity, 2017 Apr).  Studies have identified that elevated small-dense LDL cholesterol correlates much more closely with risk for inflammation, heart disease and vascular disease (Williams PT, et al. Atherosclerosis. 2014 April; 233(2): 713-720.)

A Better Marker for Heart Disease Risk?

Recent research demonstrates that small dense LDL cholesterol is a better marker for prediction of cardiovascular disease than total LDL-C (Hoogeveen RC et al., Arterioscler Thromb Vasc Biol. May 2014, 34(5): 1069-1077l; Ivanova EA et al., Oxidative Med Cell Longev. 2017).

The 2015 British Medical Journal, referenced above, analyzed the relevant 19 peer reviewed medical articles that included over 68,000 participants.  This review showed that there is no association of high LDL-C with mortality (meaning that an elevated LDL-C does not lead to an increased risk of death from heart or vascular disease).

In stark opposition to the landmark evidences above, the American Heart Association’s Presidential Advisory published their position in the June 20, 2017 issue of Circulation.  I am well aware of their position.  They claim that saturated fat is the cause of increased LDL-C.  Further, they extrapolate that elevated LDL-C is associated with increase in cardiovascular disease death.  This boldfaced claim is based on one single small four-year (2009-2013) literature review completed by the World Health Organization.  It looked at very small studies lasting only 3-5 weeks and comprised in total only 2353 participants.  That’s not nearly long enough to see fully effective cholesterol changes.  And, none of the studies had any focus on carbohydrate intake, insulin levels or LDL sub-particle measurement (Mensink RP, Geneva: WHO Library Cataloguing-in-Publication Data, 2016).

Clinical Evidence Is Pointing to Ketogenic Lifestyles as a Key

In my office, I see up to 10% regression in carotid stenosis (blockage in the carotid arteries) each year when following a ketogenic dietary lifestyle.  Evidence points out that higher fat intake and lowering of carbohydrate intake has a regression effect on plaque and thickness of the arterial wall. (Shai I et al., Circulation, Mar 2010.) And, increased small dense LDL cholesterol correlates with thickening of the carotid arterial wall (Gentile M et al., Clinica Chimica Acta,Naples, Italy Division of Cardiology, Nov 2013, DOI: 10.1016 / j.cca.2013.08.010)

Based on the large body of evidence that sits before us today, the use of total cholesterol and LDL-C to determine vascular disease risk are obsolete and ineffective tools.  That’s why we focus on insulin, triglycerides and small dense LDL particles.

Are you worried about your cholesterol?

Is a ketogenic lifestyle right for you?

These are great questions that I hope I can answer.  Check out this month’s Kickstart program if you’re just getting started.  Or, click here to work with me individually on your ketogenic lifestyle and cholesterol.



8 Reasons You Can't Lose Fat #DocMuscles #KetonianKing

Eight Reasons You Can’t Lose Fat

Inability to lose weight is the most common reason people see me. It’s often a combination of small things that they are unaware of that is keeping the spare tire inflated around the waist.  I’ve listed the eight most common reasons you can’t lose fat that are seen in my office.

You Eat Too Many Carbohydrates

About 85% of the people that walk through my office doors have some degree of insulin resistance. This means that they produce 2-20 times the normal amount of insulin in response to ANY form of starch or carbohydrate. Insulin is the hormone responsible for letting glucose into the cell to be used as fuel. More importantly, it is the hormone responsible for dampering glucose production in the liver and, it is the primary hormone responsible for pushing triglycerides into the fat cells (essentially, the master hormone for making you FAT). The more insulin you make the more fat you store. Insulin resistance, the inability for insulin to signal glucose dampering at the liver receptors, is the first stage that starts 15-20 years before you become a diabetic.

#DocMuscles #KetonianKing #WeaponOfMassDestructionIn order to lose fat, you have to decrease the insulin to a basal level. If you don’t the fat enters the fat cell faster than it exits and the fat cells get bigger. This is RULE number one to weight loss. You gotta turn down the high insulin surge that 85% of us are really good at producing. If you don’t do this, it is almost impossible for many of us to lose weight.

For at least 1/3rd of the people I see, this cannot be accomplished unless TOTAL CARBOHYDRATES are decreased to less than 20 grams per day. Yes, you read that correctly . . . Less that 20 grams per day.

  • Your banana contains 30 grams of carbohydrate
  • Your yogurt has up to 60 grams of carbohydrate
  • That oatmeal you thought was good for you has up to 200 grams of carbohydrate
  • The half and half you put in your coffee is half lactose (sugar from milk), 10 grams per cup.

You Eat Too Much Protein

Yes, protein can cause weight gain. There is always a body builder that sends me a nasty message after I say this, but it is true. (I’ll keep an eye on my e-mail).

#EatMoreChicken #DocMuscles #KetonianKing #TooMuchProtein

Five of the ten essential amino acids stimulate an insulin response. Remember why carbohydrates cause weight gain . . . ? (I will give you a hint . . . INSULIN).

Certain amino acids that make up proteins can do the same thing. Arginine, Lycine, Phenylalanine, Leucine & Tyrosine, in that order, stimulate insulin (1). We need protein to stay healthy, but too much of these amino acids in someone who is insulin resistant will inhibit weight loss and stimulate fat gain.

So, what foods contain these in the highest amounts? Sea lion liver (I know, this won’t go over very well with the polar bears), soy protein isolate, crab, shrimp, sesame flour, turkey breast, pork loin (it’s the leanest cut of pork – No. BACON is fine), chicken, pumpkin seeds, soybeans, peanuts, spirulina (blue green alge that is found in the sea). Yes, I get it. We’ve been told these were the healthy foods for the last 50 years. But, think about it, when did we start gaining weight as a country? 50 years ago.

Too much chicken, shrimp, crab and soy foods will inhibit weight loss in those with insulin resistance. So, consider whether it should be chicken you add to your salad. Consider, instead, bacon or beef as a wonderfully tasty substitute.

How much protein do you need?  My formula for calculating your individual amount is here in my blog Calculating Protein Needs.

You Don’t Eat Enough Fat

#Snaccident #DocMuscles #KetonianKing #BaconBoy

To successfully lose fat on a ketogenic diet, 60-70% of your caloric intake should come from fat. Yes. You read that correctly.

If we limit carbohydrates (which is currently 80% of the body’s fuel on the standard America plate), and moderate excessive protein which also halts weight loss, you have to replace the fuel. That fuel replacement should come from fat.  Increasing fat will improve the sensation of fullness, provide all the fat soluble vitamins, and actually makes food taste good again.

As long as you are lowering the insulin to basal levels, you can actually eat all the fat for which you are hungry. Add bacon, butter, coconut oil, avocado, hard cheese, and oh, did I say bacon?

But Dr. Nally, what about all that saturated fat?

The saturated fat is only a problem with vascular disease, cholesterol and heart disease when the insulin level is also high at the same time. It’s the high insulin in the presence of large amounts of fat that drives the risk for atherosclerosis (vascular and heart disease).  Instead of cutting out the fat, we’re cutting out the insulin.

How much fat should you be eating? Shoot for 60-70% of your calories from fat.  If your fat grams are slightly higher than your protein grams, you’re there. Listen to your body and eat fat until you’re full. That’s how most of my patients gauge their need and suppress hunger.

You’re Drinking Tea

Black Tea #KetonianKing #DocMuslces #WeightLoss #KetosisI know, I know.  Tea is a national pass time in Europe. And, it is deeply embedded in the culture of many other countries.  I’m probably not winning any friends across the pond by saying this, and it may bring back memories of the Boston Tea Party.  However, the problem is that leaf based teas stimulate a rise in insulin (not taxes).  I have had many patients hit a weight loss plateau because of the use of tea, specifically black tea, oolong tea, and green tea (2,3,4).

Yes, I am well aware of the tremendous benefits of the epigallocatechin gallate (ECGC) found in green tea. ECGC, which can be isolated as an extract, improves insulin resistance and improves GLP-1 signaling.  ECGC has, also, been show to improve triglycerides (5).  For this reason, it is one of the components in the KetoEssentials Multi-Vitamin I developed a few years ago and recommend to all my patients.

It appears, however, that the theaflavin within the leaf of the tea may be playing the offending role in the insulin spike seen with their use (6).

You Don’t Get Enough Sleep

Lack of sleep has been implicated in difficulty with weight loss and weight gain (7). Lack of sleep places the body into a state of chronic stress. This elevates cortisol, lowers testosterone, increases insulin (there’s that insulin problem, again) and increases the other inflammatory hormones. This perfect storm of stress, driven by lack of restful sleep, plays a big role in fat loss.

My average patient needs at a minimum of 6-7 hours of restful sleep to maintain and lose weight.

This is where untreated sleep disorders like sleep apnea play a big role. If you have sleep apnea, get it treated. What else can you do to help improve sleep?

  • Remove the computer, iPad and cell phones from the room.
  • Lower the room temperature. Men sleep better around 68-70 degrees F and women sleep better when the temperature is <70 degrees F.
  • Close the blinds or shades to add or darken the room.
  • Don’t study or watch TV in the same room you sleep in. Your body gets used to doing certain activities in certain rooms of the house. The bedroom should be reserved for sleep.
  • Go to bed at the same time
  • Get up at the same time.

It may take your body and body’s biorhythm 3-4 weeks to adjust to changes you make around sleep habits. Be patient with yourself.

You’re Married to Stress

Just as lack of sleep is stressful, other forms of chronic stress also raise cortisol, insulin and the inflammatory hormones. Chronic stress also lowers testosterone. It, also, has the potential to lower neurosignaling hormones in the brain like serotonin and dopamine, putting you at greater risk for depression and anxiety.

Other forms of chronic stress can occur from poor relationships, chronic pain, stressful employment, unfulfilled expectations, chronic illness and all forms of abuse. If any of these are playing a role in your life, you need to address them, and address them now.

As a physician, my job is stressful. Dealing with life and death issues with multiple people through the day, six or seven days a week, takes it’s toll. I’ve found that weight lifting, horseback riding, and taking care of my animals are my outlets. Find something physical, that takes you outside in the elements and forces you to break a sweat for 15-20 minutes is the key.

#FightOrFlight #DocMuscles #KetonianKing Bear Chasing ManOur bodies have a “fight or flight system.” 100 years ago, the stress was fighting or running from the bear that squared off with you when you happened upon him in the woods. Cortisol, adrenaline, epinephrine, insulin, glucose, and inflammatory hormones pour into the blood stream.  The heart beats faster, blood flows rapidly to the muscles, sensory awareness is heightened in the brain and increased oxygen flows to the lungs. This lets you fight the bear or run from the bear.

But, you can’t fight or run from your cynical boss. You can’t fight or run from oppressive finances, the person that cuts you off on your one hour commute in traffic, or your coworker who keeps pestering you. However, your body still releases adrenaline, cortisol, epinephrine, insulin and a number of inflammatory hormones prepping you to fight or run. If you don’t burn these hormones off, they halt weight loss, and actually can cause weight gain, increase anxiety and over time disrupt sleep.

So find your favorite way of physically relieving stress, and do it 2-3 times per week. (No, gentlemen, sex doesn’t count).

You Have An MTHFR Deficiency

In the last few years, we’ve been able to identify a number of genetic deficiencies that play a role in weight gain. One of those is an methyl-tetrahydrofolate enzyme deficiency (MTHFR deficiency for short). This is a genetic deficiency in the enzyme that converts adds a methyl ion to the folic acid in the cells of your body.

This is important, because if you can’t methylate folic acid inside the cell, you’ll have difficulty using vitamin B12 and B6 very efficiently to form methionine (a key amino acid in blood vessel and nerve function). There are two genes that encode for the enzyme that does the methylation of folic acid. Deficiency in one or both of these can lead to problems.

In severe cases, it causes homocysteine to build up to unsafe levels in the blood and slow the formation of methionine.  It is associated with B12 deficiency, weight gain, fatigue, migraines, depression, anxiety, neuro-developmental disorders like autism, pregnancy loss, blood clots and neuropathy in pre-diabetic and diabetic patients (8, 9, 10).

Giving extra vitamin B12, B6 and folic acid (vitamin B9) doesn’t appear to help.  Clinical evidence is pointing to the pre-methylated form of the folic acid.  Finding this pre-methylated form has been difficult and notably expensive for patients. I found this deficiency to be so prevalent in my office, I added methylated folic acid to the KetoEssentials Multivitamin.

You Give “Couch Potato” A New Name

We have become a very sedentary people. We have engineered physical activity out of our lives. Remote controls, elevators, escalators, people movers, and automation have made our lives physically easier.

The average office worker burns 300 kcal per day sitting at a desk on a computer. The average farm worker burns 2600 kcal per day. That’s the equivalent of running a marathon every day.

Physical activity doesn’t necessarily cause weight loss.  However, physical activity changes the hormones of the body including increasing a hormone called atrial naturitic peptide (ANP).  ANP opens the fat cell, and lets more fat out (11).

When physical activity is paired with the correct diet, the weight come off.  This is where exogenous ketones may play a role.  The increased presence of ketones in the blood increases the release of ANP helping to activate triglyceride release from the fat cell.

Don’t get me wrong, many of my patients can lose weight with just dietary carbohydrate restriction alone, however, if you’ve hit a stall, you may need to look at your physical activity levels and the addition of exogenous ketones.

Kickstart Ketosis over the Plateau

Is your fat loss on a plateau?  Knowing that these challenges plague people over the coming holidays, and, seeing people get hung up on these issues, I’ve created the Keto Kickstart program for the month of October.  This package provides 30 days of ketogenic essentials including vitamins, exogenous ketones and private interaction with me through the month of October to help you get over the plateau and breeze through the holidays.

Click on Kickstart to find out the details, join me next month and let me help you bridge the weight loss chasm!


  1. Floyd J et al., Stimulation of Insulin Secretion by Amino Acids, Journal of Clinical Investigation. 1966. 45(9).
  2. Bryans JA et al., Effect of black tea on post-prandial glucose and insulin. Journal Am Coll Nutrition 2007, 25(5): 471-7.
  3. Store KS & Baer DJ. Tea consumption may improve biomarkers of insulin sensitivity and risk factors for diabetes. The Journal of Nutrition. Aug 2008, 138(8): 1584S-1588S.
  4. Hosoda K et al., Anti-hyperglycemic effect of oolong tea on type II diabetes. Diabetes Care. Jun 2003. 26(6): 1714-1718.
  5. Chia-Yu Liu,Chien-Jung Huang, Lin-Huang Huang, I-Ju Chen, Jung-Peng Chiu, Chung-Hua Hsu.  Effects of Green Tea Extract on Insulin Resistance and Glucagon-Like Peptide 1 in Patients with Type 2 Diabetes and Lipid Abnormalities: A Randomized, Double-Blinded, and Placebo-Controlled Trial. PLOS one(online). March 10, 2014.
  6. Cameron, Amy R.; Anton, Siobhan; Melville, Laura; Houston, Nicola P.; Dayal, Saurabh; McDougall, Gordon J.; Stewart, Derek; Rena, Graham (2008). “Black tea polyphenols mimic insulin/insulin-like growth factor-1 signalling to the longevity factor FOXO1a”. Aging Cell. 7(1): 69–77.
  7. Beccuti, Guglielmo, and Silvana Pannain. “Sleep and Obesity.” Current opinion in clinical nutrition and metabolic care 14.4 (2011): 402–412. PMC. Web. 18 Sept. 2017.
  8. Divyakolu S, Tejaswini Y, Thomas W, Thumoju S, et al. (2013) Evaluation of C677T Polymorphism of the Methylenetetrahydrofolate Reductase (MTHFR) Gene in various Neurological Disorders. J Neurol Disord 2:142. doi: 10.4172/2329-6895.1000142
  9. Gilbody, S., Lewis, S. & Lightfoot, T. (2007). Methylenetetrahydrofolate reductase (MTHFR) genetic polymorphisms and psychiatric disorders: A HuGE review. American Journal of Epidemiology, 165(1), 1-13.
  10. Menon, S., Lea, R., Roy, B., Hanna, M., Wee, S., Haupt, L., & … Griffiths, L. (2012). Genotypes of the MTHFR C677T and MTRR A66G genes act independently to reduce migraine disability in response to vitamin supplementation. Pharmacogenetics And Genomics, 22(10), 741-749.
  11. Lafontan M et al., Control of lipolysis by natriuretic peptides and cyclic GMP. Trends in Endocrinology and Metabolism. 19(4): 130-137.