How to Make Ghee

I make ghee regularly to have on hand at home. It’s got a great flavor and a high heat point so is perfect for cooking eggs or sautéing brussel sprouts for LCHF and keto. Since it removes the milk protein, ghee is Whole30 approved.

Here’s my latest batch.

Another advantage is that it is stable at room temperature for several weeks or longer, especially in these small mason jars which seal as they cool. This makes it great for camp cooking in the RV.

I’ve also started making flavored ghee. Here are my recent creations of garlic-basil and turmeric-curry. They have a great through and through flavor. Notice that the ghee solidifies and becomes opaque when it is stored in the refrigerator.

Ghee is very easy to make. Below is an article to walk you through the steps.

I’ve started using a thick bottomed tea kettle to boil the ghee. It keeps the bottom for scorching as easily and, if you’re careful, allows for you to pour off the ghee directly into the containers without straining it.

Finally, I have two bits of advice. First, don’t turn up the heat too high or the solids at the bottom can create a strong scorched nutty flavor. Second, leave it alone until it froths up a second time. It won’t be ready until then.

Hope you enjoy it as much as I do!

Learn how to make ghee (aka liquid gold), how long homemade ghee lasts, and what its health benefits are.
— Read on

When fasting is more than going without food

If you are like most people, then you’ve heard the buzz recently on fasting but don’t quite understand the process.  If fasting is nothing more than not eating food, you could be left wondering why anyone would think this concept is a good idea or why it has developed a large, trendy following.  However, the science of fasting is starting to come to light and the health benefits are being elucidated.  It seems like this ancient ritual has hit a modern day stride.

Fasting has been part of my religious tradition for millennia, but, I admit, I have rarely practiced it.  As an evangelical Christian of the reformed tradition, I have always viewed fasting as one of those extra things you could do but it wasn’t required for salvific faith.  So over the years I would engage in types of fasting such as abstinence from particular foods during the Lenten season but never with a mindset that it might be beneficial for my physical body or that it would be very easy.  In fact, it was supposed to be hard.  I viewed it as solely an act of self-denial that was meant to sharpen my appreciation and understanding of Christ’s self-denial and sacrifice.  For me, giving up food was always a challenge.

This article from Science does a good job a describing the four basic types of fasting methods that are commonly researched.  In my practice, I typically only utilize two of them for myself and my patients.  I encourage time restricted feeding (TRF or sometimes called time restricted eating, TRE) for virtually all of my patients from day one.  As patients progress or if they have more metabolic challenges to overcome like diabetes, I will layer on intermittent fasting (IF) to their therapy plan.  Of note, the last two patients I’ve had who reversed their diabetes utilized both TRE and IF regularly.

The other two types of fasting are not as well utilized in my practice for separate reasons.  Calorie restriction has long been the cornerstone of weight loss therapies however we also have a long history of poor success with these programs.  It turns out that humans have a really hard time not eating enough food indefinitely.  Go figure.  These programs often fail because our lack of willpower to deny ourselves something we need to survive for an indeterminate time.  That is why fasting on an intermittent basis works.  We can deny ourselves for shorter periods of times, even a few days in a row, without the same psychological stress of long term food denial.  So, while calorie restriction has its scientific success stories, from a practical standpoint, I don’t find it useful in my practice.

The fasting-mimicking diet is a fascinating plan which I have yet to incorporate in large scale to my practice.  The 5 day time frame of very little food intake is a big step for many patients.  The results are impressive in animal models and the regenerative powers of such a program are hard to ignore.  I hope as our experience in fasting grows that I’ll be able to incorporate this into the appropriate patient’s therapeutic strategy.

Now, let’s go back to the two types of fasting protocols I regularly prescribe.  Time restricted eating is a very simple program where patients develop a diurnal pattern of eating for a set number of hours followed by abstinence of all food and drink save water for the remainder of there 24 hour cycle.  In several observational studies on eating schedules it has been found that many people eat some type of food every few hours from the time they get up to right before they go to bed.  That accounts for up to 16 hrs out of every 24 that we’re ingesting something.  The 7-8 hour window of bedtime and sleep is the only time they don’t consume food.

F3.largeWith TRE that 7-8 hour window of fasting is stretched so that the minimum fasting time to be considered TRE is about 12 hours.  Biologically, many unique activities begin to occur after 12 hours of fasting that don’t occur while we are in the fed state.  As the duration of fasting grows, the cellular changes continue to expand such that after 13-14 hours of fasting several thousand fasting-only cellular activities are occurring.  If we never reach this threshold, then we can never see the effects.

For most all of my patients, I recommend TRE of about 12 hours as a basic step.  It’s not too hard either.  Most patients have to decide not to eat again after dinner by avoiding their bedtime snack.  Breakfast may need to be pushed back to sometime other than upon awakening in the morning.  Otherwise, many patients don’t require much adaptation.  This type of fasting doesn’t require much in the way of nutrient change either.  Therefore, as patients learn to change their nutrition some simple changes in timing can be incorporated too.

As patients progress in our dietary education program and adopt our whole food, low carbohydrate, high fat approach I encourage them to incorporate intermittent fasting (IF) into their weekly schedule.  By the way, the graphic above lists the low carb, high fat (LCHF) approach as ‘obesogenic’.  This is blatantly wrong on several levels but I won’t address it in this post.  Not coincidentally, as this nutrition program takes root in a person’s daily life, their body begins to normalize hormonal production of insulin, grehlin, and leptin.  These regulatory hormones help us shed or store weight and strongly influence the hunger sensation.  Normalization allows for weight loss which prompts reduced hunger.   Consider this, if stored weight in a fat cell is being released into the blood stream and your body is now tuned to utilize that for fuel, wouldn’t the need for finding food to ingest lessen?  It does, dramatically.

As patients adopt and adapt to the whole food, LCHF plan, they naturally adopt varying degrees of TRE and IF.  They often forget to eat.  They get busy working on something and without the hunger drive to kick in they opt to work through the day instead of stopping for lunch.  It’s not that their mechanisms are broken, it’s just that their fuel tanks are so much bigger now.  They don’t run out nearly as easily.

As this progresses, I encourage my patients to find one 24 hour stretch of time that they can fast.  Often the best time to do this is the roughly 24 hours that begins after a dinner meal and ends prior to the next meal.  By skipping after dinner eating and snacks, we can wake up with 10-12 hours of fasting already out of the way.  We’re well into the cellular machinery that makes fasting easier.  Continuing this until the dinner meal will be less challenging than you think.F4.large

I’ve talked a lot about the types of fasting I use in my practice and touched slightly on how to initiate them.  However, there are many factors involved which I obviously can’t cover in a blog post.  Please don’t take this as specific medical advice for you in your situation as many other factors need to be considered.  If you’re on medications that are influenced by fasting, you’ll need advice on how to adjust them.  If one fails to appropriately adjust their insulin, for instance, it could be disastrous or even deadly for someone attempting to fast.

If you’re interested in adding fasting to your dietary regimen, then give me a call.  As a DPC patient you already have my phone number and email so feel free to contact me anytime.  The DPC dietician, Carly Slagle, and I will guide you through a program that makes sense and allows you to hit your health goals.  If you aren’t a member of our DPC program, then consider signing up.  It’s hard to imagine just how healthy you can be until you start to see the progress that so quickly occurs with good nutrition.

Hard work beats Big Pharma. Every time.

Wow! Just wow!
My patient’s Hgb A1c went from 13.5% to under 7% with a little free metformin and lots of low carb, healthy fat (LCHF) hard work in just 7 months.
Beat that Big Pharma! 
I’m so proud of them.  It is just a joy to walk with my patients as they get healthier and healthier.
-Dr. McColl

10 Paleo Thanksgiving Recipes to Delight the Pickiest Eaters | MyDomaine

Instead of crossing your fingers for at least one edible dish this Thanksgiving, ask your host if you can prepare one of these paleo Thanksgiving recipes.
— Read on

Anti-aging molecule produced by fasting

A recent study showed that the effect of aging on arteries can be delayed by a molecule your body makes during a fasting.

Fasting-induced anti-aging molecule keeps blood vessels young

When the body fasts from food intake it enters a unique period that restores and resets many of the normal body functions.  The general flow of energy shifts from a net storage mode to a net utilization mode.  Energy, often in the form of triglycerides, having been cleared from the blood stream by a few hours of no food intake is now being called out of storage to fuel various organ systems.  As the triglycerides come out they are converted into three ketone byproducts; one of which is beta-hydroxybutyrate.  This particular molecule was shown to induce cell growth and proliferation within the vascular system in a recent study.  Rejuvenation of the cells within a blood vessel can help keep them flexible and compliant as opposed to the chronic pressures for them to stiffen and calcify during atherosclerosis.

Ketones and ketosis have had a bad rap over the years but as research and experience progresses, we see many beneficial effects.  It is something I teach regularly to my patients and have found it to be a powerful tool that can reverse diseases like diabetes, high blood pressure, and high cholesterol.  Weight loss is a given with measurable ketosis but, more importantly, people feel so much better.

Consider what a primary care practice dedicated to proper nutrition AND exceptional medical care could do to help you reach your health goals.  Don’t let an eight minute appointment turn into a lifetime of prescriptions.  Find a physician with a heart of a teacher who can help you understand how medications might not be necessary with a few simple changes.  Contact our office for more information on our nutritional education program.



Opinion: “Carbs, Good for You? Fat Chance!”

Nina Teicholz, author of The Big Fat Surprise, published an opinion piece in the Wall Street Journal yesterday concerning the recent ‘low carb equals an early death’ study.  Junk science and flashy headlines are really bad for public health.  Let’s focus on good studies that show causal effects.

What I see every day in my practice is how good nutrition reverses and cures many chronic diseases, restores vitality and health, and allows patients to regain their lives.

Carbs, Good for You? Fat Chance!

Eat real food.

Anyone that’s looked at my Wellness Prescription handout knows that the first step of good nutrition is to eat real food. After that, we need to engineer a low enough carbohydrate diet to achieve our health goals. Typically, I recommend newbies start at 100gms per day, but I always individualize that level with each patient at their office visit and adjust it as they grow in experience and success.

With all the reaction to the new ‘low carb is killing you’ study, I liked what cardiologist Aseem Malhotra, MD had to say about it during a recent interview. Essentially, eating fake food is always not good for you even if you are generally low carb. However, real food that is low carb is the best of all. If you don’t know what that is or how to implement it in your life, come see us at Trinity DPC. We talk about this stuff all the time.

We have two upcoming ‘Food as Medicine’ discussions that are free for members and $20 a person for non-members.  Carly Slagle, RD and Dr. Hone are hosting a meeting in Maryville on August 23rd from 12 to 1pm.  In Hardin Valley, Carly and I will be hosting a discussion on September 4th from 1 to 2pm.  Call our office you have any questions.

How a Low-Carb Diet Might Aid People With Type 1 Diabetes – The New York Times

How a Low-Carb Diet Might Aid People With Type 1 Diabetes
— Read on

Here is a very encouraging observational study on treating Type I diabetes, those that produce little to no insulin due to a failure of their pancreas typically at a young age, with a low carb diet. The results are good and not unexpected in my experience.

I see phenomenal improvements in health, blood sugar control, and reductions in medication use when my patients adopt the low carb, ketogenic meal plan taught at Trinity.

Editorial: Added Sugars Drive Coronary Heart Disease

This is a good editorial so I’ve quoted it in its entirety.

‘I know of no single acceptable study that shows a high intake of sugar in a population that is almost entirely free from heart disease.’1—John Yudkin

Coronary heart disease (CHD) is responsible for one in every six deaths in the USA,2 and it eventually manifests as an acute myocardial infarction (MI). In the USA, almost 1 million acute MIs occur each year2 with approximately 15% of patients dying as a result of their acute event.2 If one manages to survive an acute MI, depending on the age of onset, the average survival time ranges anywhere from just 3.2 years to up to 17 years.2 Thus, CHD and acute MI are leading causes of early mortality in the USA.2

Asymptomatic hyperglycaemia is a risk factor for cardiovascular disease (CVD) and CHD, as well as death from CHD.3 Hyperglycaemia can develop during an acute MI, even in patients without diabetes,3 which may be caused by an increase in catecholamines, a reduction in the release of insulin, development of insulin resistance and increases in cortisol and growth hormone.3–5 However, many patients with MI already have diabetes and simply have yet to be diagnosed (ie, latent diabetes), where the acute stress worsens their diabetic state leading to hyperglycaemia.3 Indeed, one study showed that 73% of patients presenting with an acute MI have abnormal glucose tolerance, with 50% having diabetes.6 After 6 months, 43% still had abnormal glucose tolerance, which is approximately threefold higher than that found in matched controls (15%), the difference between the two being significant.6 Thus, hyperglycaemia does not seem to be an acute or temporary finding in patients who have experienced an MI, with many of these patients having continued abnormal glucose tolerance even when followed for several years after their event.

The Whitehall study, a prospective cohort study encompassing 18 403 patients, showed that blood glucose after a 2-hour oral glucose tolerance test was related to the age-adjusted CHD mortality after 7.5 years.7 In non-diabetics, a 2-hour blood glucose at 96 mg/dL or higher was associated with a twofold increased risk of CHD mortality.7 An elevated insulin response to an oral glucose load has been found in patients with atherosclerosis of the peripheral, cerebral and coronary arteries.8 9 In the Busselton, Australia study, insulin levels 1 hour after ingesting a 50 g oral glucose load were significantly related to the 6-year CVD incidence and 12-year CVD mortality in men aged 60 and older.10 In both the Helsinki policeman study11 and the Paris civil servant study,12 insulin levels taken in the fasting state after an oral glucose load (75 or 90 g) were associated with the occurrence of MI and CHD death 5 years later in men aged 30–59. However, the insulin:glucose ratio had the closest association with CVD. In all three studies, the relationship of insulin with CVD was independent of other covariates, including lipids, blood pressure and blood sugar.13 Considering that refined sugar, even when compared with starch, has been found to raise serum insulin levels,14 15 this provides compelling evidence that overconsuming added sugars (sucrose or high-fructose corn syrup) may lead to an increased risk of CHD through raised insulin levels.

The evidence incriminating insulin and carbohydrate in atherogenesis is strong, and that this scheme would link atherosclerosis with diabetes, obesity, hyperlipaemia, lack of physical exercise, and, possibly, hypertension.16 (Stout and Vallance-Owen)

It has been known for over 50 years that people with hypercholesterolaemia and hyperlipaemia generally have abnormal carbohydrate metabolism, with an elevated insulin level often driving their hyperlipidaemia.17 Indeed, insulin has been found to increase lipogenesis18 and stimulate smooth muscle cell proliferation.19–21 Hyperinsulinaemia is also an independent risk factor for CHD,10 11 and insulin resistance predicts future cardiovascular risk.22 23 Increased levels of insulin are found in multiple disease states, including obesity, coronary artery disease, hypertension, peripheral vascular disease and those with hypertriglyceridaemia.24 Thus, any dietary factor that worsens glucose tolerance or promotes insulin resistance will also likely increase the risk of acute MI, CHD and CHD mortality. Considering that a diet high in added sugars (particularly the fructose component) leads to insulin resistance,25–28 the overconsumption of added sugars is undoubtedly a contributing factor to CHD and CVD mortality. Indeed, compared with a diet that contains less than 10% of calories from added sugars, a diet containing 25% or more calories from added sugars nearly triples the risk for CVD mortality.29

Data from animal and human studies have noted that the isocaloric replacement of starch, glucose or a combination of both, with sucrose or fructose, increases fasting insulin levels,14 15 reduces insulin sensitivity,25–27 increases fasting glucose concentrations,30 increases glucose and insulin responses to a sucrose load14 15 and reduces cellular insulin binding.25 In other words, calorie for calorie, consuming added sugars is more harmful than starch or glucose regarding worsening of insulin sensitivity and glucose tolerance. Additionally, feeding rats sucrose leads to impaired glucose tolerance31 and adipose tissue that is less sensitive to the effects of insulin.32 33 Thus, data from animals and humans indicate that overconsuming added sugars drives insulin resistance and hyperinsulinaemia.

During an acute MI, the heart switches from primarily using fatty acids as energy to using glucose. As insulin facilitates glucose uptake into cells, patients with insulin resistance during an acute MI will have a worse prognosis. Indeed, the degree of insulin resistance is related to the severity of an MI,34 and after an MI diabetics are more likely to die compared with non-diabetics.35 A diet high in added sugars promotes insulin resistance and diabetes,14 15 28 36 37 and thus may lead to larger MIs and increase the risk of CHD mortality.

It is well known that those with diabetes have a higher risk of mortality and MI versus those without diabetes,38 which is independent of smoking status, cholesterol levels, blood pressure and body fat distribution. Additionally, patients diagnosed as being newly diabetic also have an increased risk of MI. Diabetics also have more coronary atherosclerosis than non-diabetics,39 40 particularly a higher frequency of severe narrowing of the left main coronary artery and healed transmural ventricular scars.41 The Framingham study showed that those with diabetes have an approximate threefold increased risk of dying from CVD versus the general population as well as an increased risk of stroke, CHD and peripheral arterial disease.42 Higher blood pressure or higher lipoproteins did not account entirely for the increased incidence of CHD among diabetics.13

A diet high in added sugars has been shown to increase the prevalence of diabetes, whereas a lower intake has the opposite effect.43–46 Thus, added sugars promote an increased risk of CHD by increasing the risk of diabetes, which has been shown in both ecological analyses as well as clinical trial data. Considering that added sugars also promote insulin resistance, and those who experience an acute MI are more likely to be insulin resistant, the overconsumption of added sugars drives CHD.25 27

A raised cholesterol level is not the only risk factor in those with CHD. Indeed, many other abnormalities commonly occur such as elevated glucose, insulin, triglycerides, uric acid and lower levels of high-density lipoprotein cholesterol.47 Additionally, impaired glucose tolerance, insulin resistance and altered platelet function are commonly found in patients with CHD or those with risk factors for CHD.48–51 All of these CHD abnormalities are induced or worsened in humans and animals when given a diet high in sugar,52–55 which can be reversed when reverting back to a diet low in sugar.14 55 This provides compelling evidence that the overconsumption of added sugars is a principal driver of CHD.

Administration of a diet high in sugar for just a few weeks leads to approximately one-third of men experiencing numerous changes seen in CHD and peripheral vascular disease.53 54 These suggest that the overconsumption of sugar and the subsequent insulin resistance and/or hyperinsulinaemia drive CHD as well as other diseases such as hypertension, diabetes, obesity and gout.56 57 Interestingly, smoking, which is a risk factor for heart disease, has been found to induce hyperinsulinism,58 suggesting that both the overconsumption of added sugars and smoking predispose to heart disease in a similar manner (via hyperinsulinaemia; although both also induce inflammation, oxidative stress and increased platelet adhesiveness).59–61

Over the past 200 years, the average intake of added sugars has increased from 4 to 120 lb/year.62 Sugar is even more rewarding than cocaine in animal studies, and in humans added sugar is arguably the most widely consumed addictive substance around the world.63 The fact that diabetics have an increased risk of occlusive arterial disease,24 and that non-diabetic patients with vascular disease have raised insulin levels,24 suggests that insulin resistance is at the centre of heart disease. Considering a diet high in added sugars can induce insulin resistance and hyperinsulinaemia in humans, and a reduction in added sugars can improve these metabolic derangements, there is compelling evidence that the overconsumption of added sugars (high-fructose corn syrup and sucrose) is a principal driver of CHD. Indeed, refined sugar, as compared with fat, starch, glucose, or a combination of starch and glucose, promotes greater detriments on glucose and insulin levels in humans.14 15 28 36 37

Currently, the main dietary culprit thought to lead to CHD is saturated fat. However, the overconsumption of added sugars (sucrose or table sugar and high-fructose corn syrup) has also been associated with an increased risk of CVD and mortality from cardiovascular causes. A diet high in added sugars for just a few weeks has been found to produce numerous abnormalities found in patients with CHD including elevated insulin levels and insulin resistance. More importantly, a diet low in added sugars and refined carbohydrates has been found to reverse all of these metabolic defects. The evidence indicates that added sugars are a likely dietary culprit leading to CHD.

What I Ate for Lunch

As I counsel patients about how their nutrition directly affects their health, I’m often asked questions about specific challenges.  One of the most common questions is what to eat when dining out.  I’ve decided to share some of the meals I’ve found at local restaurants that fit the low carb paradigm taught at Trinity in the hopes that it will show patients that there really are some good options when eating out.

Yesterday, I was out with my wife and son running errands and we stopped in at the Parkside Grill for a late lunch.  I had the Grilled Cilantro-Lime Chicken which comes with a rice pilaf and broccoli. I substituted the rice for green beans. It was an excellent meal; very flavorful and filling for $9.99.  Additionally, I had unsweetened ice tea, skipped the bread basket, and asked for extra butter.

I’m sure few patients are shocked that grilled chicken and green vegetables are a recommendation from their doctor in order to stick to a healthy eating plan.  However, in the midst of all the other options, even tempting salads with candied nuts, this meal was delicious, simple, and inexpensive.

The nutrient break down is listed below showing a net carb intake of 9.5 grams.

Fat 22.1g 41.9%
Saturated Fat 11.6g
Cholesterol 209.3mg
Sodium 486.9mg
Carbohydrates 15.9g 13.4%
Fiber 6.4g
Sugars 6.1g
Protein 53.1g 44.8%