Category Archives: fat

the complete guide to fasting (review)

Considering the massive amount of research and interest in the idea of fasting, not a lot has been written for the general population on the topic.

Brad Pilon’s 2009 e-book Eat Stop Eat was a great, though fairly concise, resource on the mechanisms and benefits of fasting.

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Martin Berkhan’s LeanGains blog had a cult following for a while in the bodybuilding community.

image17Michael Mosley’s 2012 documentary Eat, Fast and Live Longer documentary piqued the public interest and was followed by the popular 5:2 Diet book.

Then in 2013, Jason Fung emerged onto the low carb scene with his epic six part Aetiology of Obesity YouTube Series in which he detailed a wide range of theories relating to obesity and diabetes.

Essentially, Jason’s key points are that:

  • simply treating Type 2 diabetes with more insulin to suppress blood glucose levels while continuing to eat the diet that caused the diabetes is futile,
  • people with Type 2 diabetes are already secreting plenty of insulin, and
  • insulin resistance is the real problem that needs to be addressed.

Jason’s Intensive Dietary Management blog has explored a lot of concepts that made their way into his March 2016 book, The Obesity Code.  However surprisingly, given that Jason is the fasting guy, the book didn’t talk much about fasting.

my experience with fasting

I have benefited personally from implementing an intermittent fasting routine after getting my head around Jason’s work.  I like the way I look and perform, both mentally and physically, after a few days of not eating.  I also like the way my belt feels looser and my clothes fit better.

Complete abstinence is easier than perfect moderation.

St Augustine

I recently did a seven day fast and since then I’ve done a series of four day fasts, testing my glucose and blood and breath ketones with a range of different supplements (e.g. alkaline mineral mix, exogenous ketones, bulletproof coffee / fat fast and Nicotinamide Riboside) to see if they made any difference to how I feel and perform, both mentally and physically.

Fasting does become easier with practice as your body gets used to accessing fat for fuel.

I love the mental clarity!   My workout performance and capacity even seems to be better when I’ve fasted for a few days.

My key fasting takeaways are:

  1. Fasting is not that hard. Give it a try.
  2. You can build up slowly.
  3. If you don’t feel good. Eat!

The more I learn about health and nutrition, the more I realise how critical it is to be able to burn fat and conserve glucose for occasional use.  We get into all sorts of trouble when we get stuck burning glucose.

Our body is like a hybrid car with a slow burning fat motor (with a big fuel tank) and high octane glucose motor (with a small fuel tank).  If you’re always filling the small high octane fuel tank to overflowing, you’ll always be stuck burning glucose and your fat burning engine will start to seize up (i.e. insulin resistance and diabetes).

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Reducing the processed carbs in our diet enables us to lower our insulin levels and retrain our body to burn fat again.  But nothing lowers insulin as aggressively and effectively as not eating.

Even though lots of Jason’s thoughts on fasting seem self-evident, his blog elucidating them has been very popular, perhaps because the concept of fasting is novel in the context of our current nutritional education.

We’ve been trained, or at least given permission, to eat as often as we want by the people that are selling food or sponsored by them.[1]

context

Jason’s angle on obesity and diabetes comes from his background as a nephrologist (kidney specialist) who deals with chronically ill people who are a long way down the wrong track before they come to his office.  Jason also talks about how he had tried to educate his patients about reducing their carbs, however after eating the same thing for 70 years this is just too hard for many people to change.

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Desperate times call for desperate measures!

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Many of these patients come to him jamming in hundreds of units a day of insulin to suppress blood glucose levels, even though their own pancreas is still likely secreting more than enough insulin.

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Rather than continuing to hammer more insulin to suppress the symptom (high blood glucose), the solution, according to Jason, is to attack the ultimate cause (insulin resistance) directly.

Jimmy Moore is well known to most people that have an interest in low carb or ketogenic diets.  Whether you agree with his approach, it’s safe to say that low carb and keto would not be as popular today without his role.

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Meanwhile Jason talks about trying to educate people about reducing the processed carbs from their diet not working, not because of the science but more due to people not being able to change their eating habits after 70 years.

the Complete Guide to Fasting

You’ve probably heard by now that Jason has teamed up with Jimmy to write The Complete  Guide to Fasting which captures Jason’s extensive thoughts on fasting from the blog along with Jimmy’s n=1 experiences and wraps them up in a cohesive comprehensive manual with a colourful bow.

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Jason and Jimmy both sent me a copy of their new 304 page book, The Complete Guide to Fasting, to review (thanks guys).   So here goes…

Similar to The Obesity Code, TCGTF is a compilation of ideas that Jason has developed on his Intensive Dietary Management blog.  Blogging is a great way to get the ideas together and thrash them out in a public forum.   Some people love to read the latest blog posts and debate the minutiae, however most people would rather spend the $9 and sit down with a comprehensive book and get the full story.

Unlike The Obesity Code, TCGTF is a bright, full colour production with great graphics that will make it worth buying the hard copy to have and to hold.

TCGTF did originally have the working title Fasting Clarity as a follow on from Jimmy’s previous Cholesterol Clarity and Keto Clarity.   However, other than Jimmy’s discussion of his n=1 fasting experiences, TCGTF is predominantly written in Jason’s voice building from his blog, so it wouldn’t be appropriate for it to have become the third in Jimmy’s Clarity series.

What is similar to Jimmy’s clarity series is that it’s easy to read and accessible for people who are looking for an entry level resource.  This book will be great for people who are interested in the idea of fasting.  It is indeed the complete guide to fasting and is full of references to studies, however it doesn’t go into so much depth as to lose the average reader with scientific detail and jargon.

The book covers:

  • Jimmy’s n=1 experience with fasting,
  • Dr George Cahill’s seminal work on the effects of fasting on metabolism, glucose, ghrelin, insulin, and electrolytes,
  • the history of fasting over the centuries,
  • myth busting about fasting,
  • fasting in weight loss,
  • fasting and diabetes, physical health, and mental clarity,
  • managing hunger during a fast,
  • when not to fast, and
  • when fasting can go wrong.

The book is complete with a section on fasting fluids (water, coffee, tea, broth) and a range of different protocols that you can use depending on what suits you.  What did seem out of place are the recipes for proper meals.  Apparently, the publisher insisted they include these to widen the appeal (If you don’t like the fasting bit you’ve still got some new recipes?)

Overall, the book will be an obvious addition to the library (or Kindle) of people who are already fans of Jason and / or Jimmy and want a polished, consolidated presentation of all their previous work with a bunch of new material added.

TCGTF will also be a great read for someone who is interested learning more about fasting and wants to start at the beginning.   TCGTF is the most comprehensive book on the topic of fasting that I’m aware of.

my additional 2c…

Jason doesn’t mind weighing into a controversial argument, using some hyperbole or dropping the occasional F-bomb for effect and Jimmy’s no stranger to controversy either, so I thought I’d take this opportunity to give you my 2c on some of the topical issues at the fringe that aren’t specifically unpacked in the book.  We learn more as we thrash out the controversial issues at the fringes.   Many arguments come down to context.

target glucose levels

Jason has come under attack for using the word ‘cured’ in relation to HbAc1 values that most diabetes associations would consider non-diabetic,[2] though are not yet optimal.[3]

In the book Jason does discuss relaxing target blood glucose levels during fasting.  This makes sense for someone taking a slew of diabetic medications.   They’re probably not going to continue the journey if they end up in a hypoglycaemic coma on day one.

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The chart below shows the real life blood glucose variability for someone with Type 1 Diabetes on a standard diet.  With such massive fluctuations in glucose levels, it’s impossible to target ideal blood glucose levels (e.g. Dr Bernstein’s magic target blood glucose number of 4.6 mmol/L or 83 mg/dL).

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If your glucose levels are swinging wildly due to a poor diet coupled with lots of medication, your glucose levels are simply going to tank when you stop eating.  Hence, a safe approach is to back off the medication, at least initially, until your glucose levels have normalized.

Being married to someone with Type 1 Diabetes, I have learned the practical realities of getting blood glucose levels as low as possible while still avoiding dangerous lows.[4]  My wife Monica doesn’t feel well when her blood glucose levels are too low, but neither does she feel good with high blood glucose levels.  Balancing insulin and food to get blood glucose levels as low as possible without experiencing lows requires constant monitoring.

The chart below shows how scattered blood glucose levels can be even if you’re fairly well controlled.   Ideally you want the average blood glucose level to be as low as possible while minimising the number of hypoglycaemic episodes (i.e. below the red line).  If you can’t reduce the variability you just can’t bring the average blood glucose level down.  The last thing you want is to be eating to raise your blood glucose levels because you had too much blood glucose lowering medication.

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Pretty much everyone agrees that it’s dumb to be eating crap food and dosing with industrial levels of insulin to manage blood glucose levels.   High levels of exogenous insulin just drive the sugar that is not being used to be stored as fat in your belly, then your organs, and then in the more fragile places like your eyes and the brain.

Jason’s perspective is that people who are chronically insulin resistant and morbidly obese are likely producing more than enough insulin.  The last thing they need is exogenous insulin which will keep the fat locked up in their belly and vital organs.  Dropping insulin levels as low as possible using a low insulin load diet and fasting coupled with reducing medications will let the fat flow out.

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fasting to optimise blood glucose levels

In the long run, neither high insulin nor high glucose levels are optimal.

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Once you’ve broken the back of your insulin resistance with fasting, you can continue to drive your blood glucose levels down towards optimal levels.

One of the most popular articles on the Optimising Nutrition blog is how to use your glucose meter as a fuel gauge which details how you can time your fasting based on your blood glucose levels to ensure they continue to reduce.

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Your blood glucose levels can help calibrate your hunger and help you to understand if you really need to eat.  I think this is a great approach for people whose main issue is high blood glucose levels and who aren’t ready to launch into longer multi day fasts.

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In a similar way, a disciplined fasting routine can help optimise blood glucose levels in the long term.  The chart below shows a plot of Rebecca Latham’s blood glucose levels over three months where she used her fasting blood glucose numbers AND body weight to decide if she would eat on any given day.

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While there is some scatter in the blood glucose levels, you can see that regular fasting does help to reduce blood glucose levels over the long term.

Once you’ve lost your weight , broken the back of your insulin resistance and stopped eating crap food, you may find that you still need some exogenous insulin or other diabetic medication to optimise blood glucose levels if you have burned out your pancreas.

fasting frequency

The TGTF book covers off on several fasting regimens such as intermittent fasting, 24 hours, 36 hours, 42 hours and 7 to 14 days.  One concept that I’m intrigued by, similar to the idea of using your glucose meter as a fuel gauge, is using your bathroom scale as a fuel gauge.

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The reality, at least in my experience, is that we can overcompensate for our fasting during our feasting and end up not moving forward toward our goal.

If your goal is to lose weight I like the idea of tracking your weight and not eating on days that your weight is above your goal weight for that day.

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Again, Rebecca Latham has done a great job building an online community around the concept of using weight as a signal to fast through her Facebook group  My Low Carb Road – Fasting Support.

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The chart below shows Rebecca’s weight loss journey through 2016 where she initially targeted a weight loss of 0.2 pounds AND a reduction of 0.25 mg/dL in blood glucose per day.   After three months, she stabilized for a period (during a period when she had a number of major family issues to look after).  She is now using a less aggressive weight loss goal as she heads for her long-term target weight at the end of the year.

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The chart below shows the fasting frequency required to achieve her goals during 2016.  Tracking her weight against her target rate of weight loss has required her to fast a little more than one day in three to stay on track.

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Eating quality food is part of the battle, but managing how often you eat is also an important consideration.  After you’ve fasted for a few days, you can easily excuse yourself for eating more when you feast again.  And maybe it’s OK to enjoy your food when you do eat rather than tracking every calorie and trying to consciously limit them.

The obvious caveat is that there are a lot of other things that influence your scale weight such as muscle gain, water, GI tract contents etc, but this is another way to keep yourself accountable over the long term.

FAST WELL, FEED WELL

Fasting is a key component of the metabolic healing process, but it’s only one part of the story.

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Fasting is like ripping out your kitchen to put in a new one.   You have to demolish and remove the old stovetop to put the new shiny one back in.  You don’t sticky tape the new marble bench top over the crappy old Laminex.  You have to clean out the old junk before you implement the new, latest, and greatest model.

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In fasting, the demolition process is called autophagy, where the body ‘self eats’ the old proteins and aging body parts.   The great thing about minimising all food intake is that you get a deeper cleanse than other options such as fat fast, 500 calories per day or a protein sparing modified fast (PSMF).

But keep in mind that it’s the feast after the fast that builds up the shiny, new body parts that will help you live a longer, healthier, and happier life.

“Fasting without proper refeeding is called anorexia.” 

Mike Julian

Even fasting guru Valter Longo is now talking about the importance of feast / fast cycles rather than chronic restriction.  In the end you need to find the right balance of feasting / fasting, insulin / glucagon, mTOR / AMPK that is right for you.

In TCGTF, Jason and Jimmy talk about prioritising nutrient dense, natural, unprocessed,  low carb, moderate protein foods after the fast.  I’d like to reiterate that principle and emphasise that nutrient density becomes even more important if you are fasting regularly or for longer periods.

In the long term, I think your body will drive you to seek out more food if you’re not giving it the nutrients it needs to thrive.  Conversely, I think if you are providing your body with the nutrients it needs with the minimum of calories I think you will have a better chance of accessing your own body fat and reaching your fat loss goals.

optimising insulin levels AND nutrient density

It’s been great to see the concept of the food insulin index and insulin load being used by so many people!  In theory, when people reduce the insulin load of their diet they more easily access their own body fat and thus normalizes appetite.

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Some people who are very insulin resistant do well, at least initially, on a very high fat diet.  However, as glycogen levels are depleted and blood glucose levels start to normalise, I think it is prudent to transition to the most nutrient dense foods possible while still maintaining good (though maybe not yet optimal) blood glucose levels.

The problem with doubling down on reducing insulin by fasting combined with eating only ultra-low insulinogenic foods is that you end up “refeeding” with refined fat after your fast.

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While lowering carbs and improving food quality is the first step, I think that, as soon as possible you should start focusing on building up your metabolic machinery (i.e.  muscles and mitochondria).   A low carb nutrient dense diet is part of the story, but I don’t see many people with amazing insulin sensitivity that don’t also have a good amount of lean muscle mass which is critical to ‘glucose disposal’, good blood sugar levels and metabolic health.

This recent IHMC video from Doug McGuff provides a stark reminder of why we should all be focusing on maximising strength and lean muscle mass to slow aging.

The chart below shows a comparison of the nutrient density of the various dietary approaches.  Unfortunately, a super high fat diet is not necessarily going to be as nutrient dense and thus support muscle growth, weight loss, or optimal mitochondrial function as well as other options.

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The chart below (click to enlarge) shows a comparison of the various essential nutrients provided by a high fat therapeutic ketogenic dietary approach versus a nutrient dense approach that would suit someone who is insulin sensitive.

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I developed a range of lists of optimal foods that will help people in different situations with different goals to maximise the nutrient density that should be delivered in the feast after the fast.   The table below contains links to separate blog posts and printable .pdfs.  The table is sorted from highest to lowest nutrient density.   In time, you may be able to progress to a more nutrient dense set of foods as your insulin resistance improves.

dietary approach printable .pdf
weight loss (insulin sensitive) download
autoimmune (nutrient dense) download
alkaline foods download
nutrient dense bulking download
nutrient dense (maintenance) download
weight loss (insulin resistant) download
autoimmune (diabetes friendly) download
zero carb download
diabetes and nutritional ketosis download
vegan (nutrient dense) download
vegan (diabetic friendly) download
therapeutic ketosis download
avoid download

protein

Jason had  a “robust discussion” with Steve Phinney over the topic of ideal protein levels recently during the Q&A session at the recent Low Carb Vail Conference.

To give some context again, Phinney is used to dealing with athletes who require optimal performance and are looking to optimise strength.  Meanwhile Jason’s patient population is typically morbidly obese people who are on kidney dialysis and probably have some excess protein, as well as a lot of fat that they could donate to the cause of losing weight.

I also know that Jimmy is a fan of Ron Rosedale’s approach of minimising protein to minimise stimulation of mTOR.  Jimmy and Ron are currently working on another book (mTOR Clarity?).  Protein also stimulates mTOR which regulates growth which is great when you’re young but perhaps is not so great when you’ve grown more than enough.

The typical concern that people have with protein in a ketogenic context is that it raises blood insulin in people who are insulin resistant.  ‘Excess protein’ can be converted to blood glucose via gluconeogenesis in people who are insulin resistant and can’t metabolise fat very well.

Managing insulin dosing for someone with Type 1 Diabetes like my wife Monica is a real issue, though she doesn’t actively avoid protein.  She just needs to dose with adequate insulin for the protein being eaten to manage the glucose rise.

The chart below shows the difference in glucose and insulin response to protein in people who have Type 2 Diabetes (yellow lines) versus insulin sensitive (white lines) showing that someone who is insulin resistant will need more insulin to deal with the protein.

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As well as insulin resistance, these people are also “anabolic resistant” meaning that some of the protein that they eat is turned into glucose rather than muscle leaving them with muscles that are wasting away.

People who are insulin resistant are leaching protein into their bloodstream as glucose because they can’t mobilise their fat stores for fuel.  They are dependent on glucose and they’ll even catabolise their own muscle to get the glucose they need if they stop eating glucose.

While it’s nice to minimise insulin levels, I wonder whether people who are in this situation may actually need more protein to make up for the protein that is being lost by the conversion to glucose to enable them to maintain lean muscle mass.  Perhaps it’s actually the people who are insulin sensitive that can get away with lower levels of protein?

As well as improving diet quality which will reduce insulin and thus improve insulin resistance, in the long term it’s also very important to maintain and build muscle to be able to dispose of glucose efficiently and also improve insulin resistance.

In TCGTF Jason talks about the fact that the rate of the use of protein for fuel is reduced during a fast and someone becomes more insulin sensitive.  He goes to great lengths to point out that concern over muscle loss shouldn’t stop you trying out fasting (which is a valid point).

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A big part of the magic of fasting is that you clean out some of your oldest and dodgiest proteins in your body and set the stage for rebuilding back new high quality parts.   But the reality is that you will lose some protein from your body during a fast (though this is not altogether a bad thing).[5] [6]

Bodybuilders often talk about the “anabolic window” after a workout where they can maximise muscle growth after a workout.  Similarly, one of the awesome things about fasting is that you reduce your insulin resistance and anabolic resistance meaning that when at the end of your fast your body is primed to allocate the high quality nutrients you eat in the right place (i.e. your muscles not your belly or blood stream).

In the end, I think optimal protein intake has to be guided to some extent by appetite.  You’ll want more if you need it, and less if you don’t.

I think if we focus on eating from a shortlist of nutrient dense unprocessed foods we won’t have to worry too much about whether we should be eating 0.8 or 2.2 g/kg of lean body mass.

However, avoiding nutrient dense, protein-containing foods and instead “feasting” on processed fat when you break your fast will be counter-productive if your goal is weight loss and waste a golden opportunity to build new muscle.

are you really insulin resistant?

Insulin resistance and obesity is a continuum.

Not everyone who is obese is necessarily insulin resistant.

If you are really insulin resistant, then fasting, reducing carbs, and maybe increasing the fat content of your diet will enable you to improve your insulin resistance.  This will then help with appetite regulation because your ketones will kick in when your blood glucose levels drop.

However, if you continue to overdo your energy intake (e.g. by chasing high ketones with a super high fat, low protein diet), then chances are, just like your body is primed to store protein as muscle, you will be very effective at storing that dietary fat as body fat.

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I fear there are a lot of people who are obese but actually insulin sensitive who are pursuing a therapeutic ketogenic dietary approach in the belief that it will lead to weight loss.  If you’re not sure which approach is right for you and whether you are insulin resistant, this survey may help you identify your optimal dietary approach.

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optimal ketone levels

Measuring ketones is really fascinating but confusing as well.

“Don’t be a purple peetone chaser.”

Carrie Brown, The Ketovangelist Podcast Ep 78

Urine ketones strips have limited use and will disappear as you start to actually use the ketones for energy.

In a similar way blood ketones can be fleeting.  Some is better than none, but more is not necessarily better.  As shown in the chart of my seven day fast below I have had amazing ketones and felt really buzzed at that point but since then I haven’t been able to repeat this.  I think sometimes as your body adapts to burning fat for fuel the ketones may be really high but then as it becomes efficient it will stabilise and run at lower ketone levels even when fasting.

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If your ketone levels are high when fasting then that’s great.  Keep it up.  They might stay high.  They might decrease.  But don’t chase super high ketones in the fed state unless you are about to race the Tour de France or if you want your body to pump out some extra insulin to bring them back down and store them as fat.

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The chart below shows the sum of 1200 data points of ketones and blood glucose levels from about 30 people living a ketogenic lifestyle.  Some of the time they have really high blood ketone levels but I think the real magic of fasting happens when the energy in our bloodstream decreases and we force our body to rely on our own body fat stores.

the root cause of insulin resistance is…

So we’ve worked out that large amounts of processed carbs drive high blood glucose and insulin levels which is bad.

We’ve also worked out that insulin resistance drives insulin levels higher, which is bad.

But what is the root cause of insulin resistance?

I think Jason has touched on a key component in that, as with many things, resistance is caused by excess.  If we can normalise insulin levels, then our sensitivity to insulin will return, similar to our exposure to caffeine or alcohol.

However, at the same time, I think insulin resistance is potentially more fundamentally caused by our sluggish mitochondria that don’t have enough capacity (number or strength) to process the energy we are throwing at them, regardless of whether they come from protein, carbs, or fat.

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A low carb diet lowers the bar to enable us to normalise our blood glucose levels.  However, the other end of the spectrum is focusing on training our body and our mitochondria to be able to jump higher.  In the long term this is achieved through, among other things, maximising nutrient dense foods and building lean body mass through resistance exercise.

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summary

  1. The Complete Guide to Fasting is, as per the title, the complete guide to fasting. It’s the most comprehensive guide to the nuances of fasting out there and there’s a good balance between the technical detail, while still being accessible for the general public.
  2. Fasting can help optimise blood glucose and weight in the long term, with a disciplined regimen.
  3. Fasting makes the body more insulin sensitive and primes it for growth. When you feast after you fast, it is ideal to make sure you maximise nutrient density of the food you eat as much as possible while maintaining reasonable blood glucose levels.
  4. Understanding your current degree of insulin resistance can help you decide which nutritional approach is right for you. As you implement a fasting routine and transition from insulin resistance to insulin sensitivity you will likely benefit from transitioning from a low insulin load approach to a more nutrient dense approach.

 

references

[1] https://intensivedietarymanagement.com/of-traitors-and-truths/

[2] https://www.diabetes.org.uk/About_us/What-we-say/Diagnosis-ongoing-management-monitoring/New_diagnostic_criteria_for_diabetes/

[3] https://optimisingnutrition.com/2015/03/22/diabetes-102/

[4] https://optimisingnutrition.com/2015/08/17/balancing-diet-and-diabetes-medications/

[5] https://www.dropbox.com/s/h3pi53njcfu4czl/Physiological%20adaptation%20to%20prolonged%20starvation%20-%20Deranged%20Physiology.pdf?dl=0

[6] https://www.facebook.com/groups/optimisingnutrition/permalink/1602953576672351/?comment_id=1603210273313348&comment_tracking=%7B%22tn%22%3A%22R9%22%7D

breakfast of champions

My Facebook feed has been flooded lately with stories about Tour de France cyclists going low carb.[1]

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Or is it high protein?[2]

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Whatever is going on, it seems helps them run well too![3]

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While I’m not sure you can say that these elite cyclists have eschewed all carbohydrate-containing foods,  the trend away from processed carbs to whole foods is intriguing.

So if they’re going low carb does it mean they’re now butter, cream, MCT oil after starting the day with BPC?

Dr. James Morton, head of nutrition at Team Sky and an associate professor in the Faculty of Science at Liverpool John Moores University explains:[4] [5] [6] [7] [8]

We promote a natural approach to food.  Our riders eat food that grows in the ground or on a tree and protein from natural sources.

They need energy, but they also have to stay lean and healthy with a strong immune system. A natural diet is the best way to achieve this.

Fat is important for everything from energy release and muscle health to immunity, but by eating the right food the fat takes care of itself.  The riders eat eggs, milk, Greek yogurt, nuts, olive oil, avocados and some red meat for a natural mix of saturated and unsaturated fats.”

To achieve optimal weight Dr Morton asks the riders to “periodise” their carb intake by eating more when they train hard and cutting back when they’re less active.

They routinely train in the morning after eating a protein-rich omelette, instead of carbohydrate-dense bread, to encourage their bodies to burn fat for fuel.[9]

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So how does low carb real food thing work?

According to Dr Terry Wahls it seems that nutrient density is a key part of maximising energy output.

To produce ATP efficiently, the mitochondria need particular things.  Glucose or ketone bodies from fat and oxygen are primary.  

Your mitochondria can limp along, producing a few ATP on only these three things, but to really do the job right and produce the most ATP, your mitochondria also need thiamine (vitamin B1), riboflavin (vitamin B2), niacinamide (vitamin B3), pantothenic acid (vitamin B5), minerals (especially sulfur, zinc, magnesium, iron and manganese) and antioxidants.  Mitochondria also need plenty of L-carnitine, alpha-lipoic acid, creatine, and ubiquinone (also called coenzyme Q) for peak efficiency.  

If you don’t get all these nutrients or if you are exposed to too many toxins, your ATP production will become less efficient, which leads to two problems:

Your body will produce less energy so they may not be able to do everything they need to do.

Your cells will generate more waste than necessary in the form of free radicals.

Without the right nutrient sources to fuel the ATP production in the mitochondria – which in turn produce energy for the cellular processes required to sustain life – your mitochondria can become starved.  The cells then can’t do their job as effectively.[10] 

So let’s look at the macro and micronutrient analysis of Chris Froome’s “rest day breakfast” (pictured above).   The analysis indicates that it does very well in both the vitamins and minerals score as well as the amino acids score.

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If we throw in some spinach Froomey would improve the vitamin and mineral score of his breakfast even further.  The addition of spinach increases the nutrient balance score from 57 to 77 while the amino acid score stays high.

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Froome’s wife says eating more protein has been one of the keys to losing weight and building muscle leading up to the tour.[11]  Getting a quarter of your calories from protein is more than the 16% most people consume, however with 65% of the energy coming from fat you could also call this meal low carb, high fat, or even “ketogenic” depending on which camp you’re in.

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This simple but effective meal would be a pretty good option for just about anyone.  Froome’s breakfast ranks well regardless of your goals.  Based on the ranking system of meals for different goals it comes in at:

  • #10 (with spinach) and #31 (without spinach) out of 245 meals analysed for the low carb diabetes ranking,
  • #18 and 52 on the therapeutic ketosis ranking, and
  • #26 and 64 on the overall nutrient density ranking.

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It seems it’s not just the low carbers, “ketonians”[12] and people battling diabetes who are training their bodies to burn fat more efficiently.  Maximising your ability to burn fat is critical even if you are extremely metabolically healthy.

The chart below shows comparison of the fat oxidation rate of well trained athletes (WT) versus recreationally (RT) athletes (who are not necessarily following a low carb diet).[13]  The well trained athletes are clearly oxidising more fat, which enables them to put out a lot more power (measured in terms of their VO2max).   It seems that you ability to efficiently burn fat for fuel it a key component of what sets the elite apart from the amateurs whether you call yourself vegan, ketogenic or a fruitarian.[14]

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While carbohydrates help to produce maximal explosive power, it seems that the glucose turbocharger works best when it sits on a big power fat fueled motor.  According to Peter Defty (who spent the last couple of years helping 2016 Tour de France second place getter Romain Bardet refine his ability as a fat adapted athlete using his Optimised Fat Metabolism protocol), fat can yield more energy more efficiently with less oxidative stress which requires less recovery time.[15]

Dr Morton also understand the importance of keeping carbohydrates low to maximise mitochondrial biogenesis and to access fat stores.  If you want to learn more about his thinking on the use of diet to drive mitochondrial biogenesis you might be interested in checking out his array of published papers on the topic.[16] [17] [18] [19] [20] [21] [22]   On the topic of carbohydrate intake Morton says:

Amateur riders are taught the importance of carbohydrates for training and racing, perhaps too much actually.

From our research at Liverpool John Moores University, we now know that deliberately restricting carbs around carefully chosen training sessions can actually enhance training adaptations.

But then of course we must ensure higher carbohydrate intakes for key training sessions and hard stages in racing.

I believe this concept of periodising daily carbohydrate intake is the most exciting part of sports nutrition in the last decade and our challenge now is to address how best we do this practically.

Essentially, exercising your mitochondria in a low insulin and low glucose state forces your body to adapt to using fat for fuel and to use glucose and oxygen efficiently and effectively.[23] [24]

image06[1]

Not only is this useful for endurance athletes and people battling diabetes, training your body to use fat and oxygen more effectively is also claimed to be important to minimise anaerobic fermentation which is said to increase your risk of cancer.[25] [26] [27]

Many of us struggle trying to cope in an environment of excess energy from low nutrient density highly insulinogenic food.  If we can’t obtain the necessary nutrients from our food to efficiently produce energy our bodies seek out more and more food in the hope of finding the required nutrients and enough energy to feel OK.

image13[1]

Our bodies do their best to use the energy that we give them, but they are working overtime to pump out insulin to store the excess energy that is not used.  Over time our bodies adapt by becoming resistant to insulin in order to stop the excess energy being stored in our liver, pancreas and eyes when our fat stores on our muscles and belly can’t take any more.[28]  Then to overcome the insulin resistance the body has to pump out more insulin which makes even less of the energy we eat available for use.

image04[1]

When we call on our mitochondria to produce intensive bursts of energy with minimal fuel (i.e. fasting) or glucose (i.e. low carb) we force our bodies to more efficiently the limited carbohydrate.  Suddenly our bodies become insulin sensitive.

Recent studies indicate that people who are fat adapted are able to mobilise higher rates of fat at higher excercise intensities.[29]

image08[2]

With a higher reliance on fat they are able to conserve the precious glucose for explosive efforts.

image02[1]

Then, when they really need the power they have both fuel tanks available to cross the  line first… and second!

image11[1]

 

references

[1] http://realmealrevolution.com/real-thinking/great-news-for-lchf-first-and-second-place-riders-of-the-tour-de-france-are

[2] http://www.businessinsider.com.au/chris-froome-weight-loss-tour-de-france-2016-7?r=US&IR=T

[3] https://www.youtube.com/watch?v=UPqxUA70ulo

[4] http://www.telegraph.co.uk/men/recreational-cycling/how-to-eat-like-a-tour-de-france-cyclist/

[5] http://www.teamsky.com/teamsky/home/article/68342#CpWWiwr2TyE0EA2P.97

[6] https://www.ljmu.ac.uk/about-us/staff-profiles/faculty-of-science/sport-and-exercise-sciences/james-morton

[7] http://www.ncbi.nlm.nih.gov/pubmed/23364526

[8] http://www.ncbi.nlm.nih.gov/pubmed/23263742

[9] http://realmealrevolution.com/real-thinking/great-news-for-lchf-first-and-second-place-riders-of-the-tour-de-france-are

[10] https://www.amazon.com/Wahls-Protocol-Autoimmune-Conditions-Principles/dp/1583335544

[11]

[12] http://ketotalk.com/2016/04/19-inflammatory-keto-foods-build-muscle-on-moderate-protein-baby-boomer-ketonians/

[13] http://m.bmjopensem.bmj.com/content/1/1/e000047.full

[14] http://www.30bananasaday.com/profile/durianrider

[15] http://www.vespapower.com/mighty-mitochondria/

[16] https://www.ljmu.ac.uk/about-us/staff-profiles/faculty-of-science/sport-and-exercise-sciences/james-morton

[17] http://ajpregu.physiology.org/content/304/6/R450

[18] http://www.ncbi.nlm.nih.gov/pubmed/23263742

[19] http://www.ncbi.nlm.nih.gov/pubmed/19265068

[20] http://journals.lww.com/acsm-msse/pages/articleviewer.aspx?year=9000&issue=00000&article=97464&type=abstract

[21] http://www.sciencedirect.com/science/article/pii/S0891584916000307

[22] http://www.tandfonline.com/doi/abs/10.1080/17461391.2014.920926

[23] https://www.fightaging.org/archives/2011/04/calorie-restriction-increases-mitochondrial-biogenesis/

[24] http://www.marksdailyapple.com/managing-your-mitochondria/#axzz4G2D39DgB

[25] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4493566/

[26] https://www.amazon.com/Tripping-Over-Truth-Metabolic-Illuminates/dp/1500600318

[27] https://www.youtube.com/watch?v=PuG5XZSR4vs

[28] http://www.ncbi.nlm.nih.gov/pubmed/25515001

[29] http://www.vespapower.com/the-emerging-science-on-fat-adaptation/

what about saturated fat?

  • The topic of saturated fat continues to be contentious.
  • While most people agree these days that minimising sugar and processed carbohydrates is a good, thing many still struggle with the idea of eating fat, particularly saturated fat.  At the other extreme there are some people who have heard the message to ‘not fear the fat’ loud and clear and seem to be making up for lost time by eating copious amounts of processed fat.
  • This article looks at what happens to nutrient density when we swing to the extremes of either very low or very high levels of saturated fat intake in our diet.  As per usual, optimal lies somewhere between the extremes.
  • If we focus on nutrient dense whole foods issues like dietary saturated fat and cholesterol tend to look after themselves.

saturated fat in various food approaches

There are plenty of different views on fat and saturated fat and very little agreement between the extremes.

If you spend much time trying to research the issue you will likely come away confused after trying to understand the implications of the epidemiological and rodent studies.

People are also very passionate on both sides of this argument.  It can be hard to know which guru to believe.

Is saturated fat the greatest dietary villain or saviour leading us from the wilderness of the low fat dark ages?

image04

You may be aware that the USDA Dietary Advisory Committee recently changed position on dietary cholesterol and removed their upper limit on fat.[1]  They did however retain their recommended upper limit on saturated fat (10% in the USA and 11% in the UK).

As noted by Dr Frank Hu in the video below, the upper limit is not based on any specific research that higher levels of saturated fat are dangerous, but rather the fact that what they consider to be healthy diets (e.g. Mediterranean, Ornish etc) were within these upper limits.

Over the last four decades massive industries have developed around the concept of lowering cholesterol in your blood through diet or drugs in order to reduce your risk of heart disease, so there is going to be a high degree of inertia that will make any change in thinking happen slowly at best.

With all the concern and confusion about saturated fat I thought it would be interesting to check the saturated fat content of the highest ranking foods identified by the food ranking system to see how they compare with the upper limits.

The table below shows that none of the food lists exceed the recommended upper limit for saturated fatty acids.  Even the diabetic friendly low insulin load approach with half the energy coming from fat has a saturated fat level less than 11%.

approach SFA fat protein insulinogenic
most nutrient dense 5.6% 22% 30% 52%
low energy density 6.9% 17% 37% 55%
low insulin load 9.7% 49% 20% 30%

So it seems that focus on nutrient dense whole foods we end with moderate, but not excessive, levels of saturated fat.[2]  

what happens if we get rid of all saturated fat?

It’s always useful to test a theory by looking at what happens at the extremes.

I starting wondering about the relationship between saturated fat and nutrient density.

“What would happen to nutrient density if you removed ALL saturated fat?”

“Does avoiding saturated fat affect nutrient density for the better or worse?”

The chart below (click to enlarge) shows the essential nutrients for foods that have no saturated fatty acids (SFA) compared to vegetables, seafood and the most nutrient dense foods.

This analysis indicates that if you eliminate saturated fatty acids the nutrient density plummets!  As you can see from the little red bars on the graph, you might be able to obtain solid levels of Vitamin C and Vitamin A from a diet with no saturated fat but everything else is abysmal!

image01

how does SFA influence nutrient density?

So eliminating saturated fat completely doesn’t appear to be such a great idea.   But what does the other extreme look like?

I sorted the 7000+ foods in the USDA database by their saturated fat content and divided them into four equal “quartiles”.  The table below shows the SFA as a percentage of calories for the different quartiles.  Interestingly, only the highest quartile exceeds the arbitrary limit for saturated fat (i.e. 13% compared to the 10% arbitrary upper limit in USA or 11% in the UK).

quartile SFA fat protein insulinogenic
first 0.05% 18% 15% 72%
second 1.1% 20% 28% 63%
third 4.5% 32% 38% 52%
fourth 13% 50% 22% 38%

I think the most interesting observation here is in the right hand column.  The more you try to avoid saturated fat the more insulinogenic your diet ends up being.  That is, in the avoidance of saturated fat you may end up exacerbating any genetic propensity that you may have towards insulin resistance and diabetes by eating foods that require your pancreas to produce high levels of insulin to keep up!

One of the challenges with the low fat approach is that the avoidance of fat can often lead to increased consumption of highly processed, highly insulinogenic foods which tend to be a problem for people who are insulin resistant.

In the 70s when they started to encourage people to eat less saturated fat (which was associated with fried junk food) people didn’t eat more vegetables as they’d hoped.  Instead people ate more processed foods that now had to be sweetened with sugar to make sure it didn’t taste like cardboard.  Some would argue that this increase in low nutrient density carbohydrates has been a major contributor to the current obesity epidemic.

image08

“Replacement of saturated fat by carbohydrates, particularly refined carbohydrates and added sugars, increases levels of triglyceride and small LDL particles and reduces high-density lipoprotein, cholesterol, effects that are of particular concern in the context of the increased prevalence of obesity and insulin resistance.”[3]

The chart below (click to enlarge) shows the nutrient density for the various nutrients for each of the saturated fat quartiles.  While it’s hard to digest all the detail on this chart it appears that, the third quartile (i.e. more saturated fat than average) tends to have the highest nutrient density on average however the second quartile is more consistently high (i.e. less highs and low).

image03

The chart below shows the average of the nutrient density across the quartiles of saturated fat.  The lowest quartile has the lowest amount of nutrients both in terms of average and being consistently high.  The foods that are the highest in saturated fat have more nutrition than the foods low in saturated fat.  However the second and third quartiles have the most.

image02

what’s the latest on saturated fat?

In this video from Dr Frank Hu points out that when you’re talking about whether saturated fat is good or bad it’s important to consider what you are exchanging it with.  For example, saturated fat is good if it’s replacing processed carbohydrates, but not so good if you are replacing your vegetables with processed saturated fat.

The most interesting paper I have found on the topic is Saturated fat and cardiometabolic risk factors, coronary heart disease, stroke, and diabetes: a fresh look at the evidence by Dariush Mozaffarin[4] which indicates that, while total cholesterol in the blood may increase with increased dietary saturated fat, the changes in HDL and total cholesterol : HDL ratio are positive.

image06

When we look in more detail it seems that saturated fats such as 14:0 and 16:0 (typically found in dairy) have positive effects on HDL and insulin sensitivity.

image05

So in the end it seems the case for or against saturated fat is confusing at best (see the Good Fats, Bad Fats article for more detail).

More recently there has been a more thorough analysis of the data from the Minnesota Coronary Experiment (1968 to 1973) on which the diet-heart hypothesis was based and which has driven the avoidance of fat in the western diet.[5] [6] [7]   The understanding based on this original research headed up by Ancel Keys, was that increased fat raises ‘bad cholesterol’ which leads to heart attacks.

Does the more rigorous analysis of the full data still support this hypothesis?    To quote from Professor Grant Schofield:[8]

The diet-heart hypothesis says that saturated fat raises cholesterol and thus causes heart disease.  Widespread acceptance of this idea has shaped the way we look and how we eat more than anything else in the history of health and medicine.

It’s still the cornerstone of conventional wisdom and dietary guidelines in virtually every country. It’s still the reason the conventional experts can’t take the biologically obvious leap to embracing low carb healthy fat diets for important treatments like weight loss and diabetes.

So, 40+ years on. Here it is in all its glory, published in the BMJ no less. What did they find?

“Available evidence from randomized controlled trials shows that replacement of saturated fat in the diet with linoleic acid effectively lowers serum cholesterol but does not support the hypothesis that this translates to a lower risk of death from coronary heart disease or all causes.

“Findings from the Minnesota Coronary Experiment add to growing evidence that incomplete publication has contributed to overestimation of the benefits of replacing saturated fat with vegetable oils rich in linoleic acid.”

That’s right, there was no support for their hypothesis in a randomised trial of more than 9500. Replacing saturated fat with Omega 6 fat did reduce cholesterol, but as we’d predict had no effect on heart disease.

The one effect they did see was that older subjects who lowered their cholesterol had higher overall mortality.  Yes, cholesterol lowering in older adults caused more death. This is an effect already seen in some population studies.

So it seems that the diet–heart hypothesis that tells us to avoid fat, particularly saturated fat, is on shaky ground these days.

so what now?

So, should we avoid fat at all costs?

image09

Or, after all these years of being told to avoid saturated fat should we rebel and make up for lost time?

image07

As with most things, optimal lies somewhere between the extremes.

Perhaps if we focus on nutrient dense whole foods then issues like dietary fat and cholesterol will look after themselves?

 

references

[1] http://www.hsph.harvard.edu/news/features/assessing-the-new-u-s-dietary-guidelines/

[2] http://daa.asn.au/for-the-public/smart-eating-for-you/nutrition-a-z/nutrient-reference-values-nrvs/

[3] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2943062/

[4] http://www.ncbi.nlm.nih.gov/pubmed/20354806

[5] http://www.pubfacts.com/detail/27071971/Re-evaluation-of-the-traditional-diet-heart-hypothesis-analysis-of-recovered-data-from-Minnesota-Cor

[6] http://whatthefatbook.com/prof-grant-on-minnesota-coronary-experiment/

[7] http://www.cbc.ca/news/health/the-case-of-the-missing-data-1.1412420

[8] http://whatthefatbook.com/prof-grant-on-minnesota-coronary-experiment/

good fats, bad fats

Even more than cholesterol or other blood markers it appears clear that insulin resistance, elevated blood glucose and hyperinsulinemia increase your risk of heart disease, obesity, stroke, cancer andom dementia.[1]

An understanding of the food insulin index data tends to lead people to increase the fat content of their diet in in an effort to normalise blood glucose and reduce insulin levels.[2]

image001

If a significant proportion of your calories are coming from fat it makes sense to look at the composition of our high fat food choices.

So let’s take a look what we could consider to be “good fats” and “bad fats” and the implications for prioritising our food choices.

a quick primer on fats

You’re likely aware that there are different classifications of fat based on their chemical structure:

  • saturated,
  • monounsaturated, and
  • polyunsaturated.

What this means is that:

  • saturated fatty acids have no double bonds between individual carbon atoms (note: saturated fats are denoted by X:0 where the X is the length of the carbon chain and 0 is the number of double bonds),
  • monounsaturated fats have one double bond (e.g. X:1), and
  • polyunsaturated fats have more than one double bond (e.g. X:2).

If you want to learn more about this topic I suggest you check out this page on nutritiondata.self.com.  It’s interesting to follow the links to see which foods are the highest in the different types of fats.

mainstream dietary advice

The standard mainstream dietary advice is to to:

  1. avoid trans fats,
  2. limit saturated fats to less than 7% of energy intake,
  3. emphasise omega 3 fats, polyunsaturated fats and monounsaturated fats, and
  4. keep dietary fat to between 20 to 35% of energy intake.[3]

The Mediterranean Diet is typically promoted as being the ideal dietary model,[4] [5] [6] although interestingly in practice people from the Mediterranean region actually consume more than the recommended amount of fat, typically from olive oils and fatty fish.[7] [8] [9] [10]

image003

dietary fats versus adipose tissue

Jeff Volek and Steve Phinney in the Art and Science of Low Carbohydrate Performance[11] [12] note that the majority of human body fat consists of monounsaturated fatty acids, with smaller amounts of saturated fats and polyunsaturated fats.  They argue that if the body stores a greater proportion of monounsaturated fatty acids for energy in times of famine then it makes sense to align our dietary fat intake with these ratios.

The table below compares the composition of human adipose tissue[13] versus the proportion of fats across the 8000 foods in the USDA database.  Based on this logic it appears that we should go out of our way to emphasis monounsaturated fat given than saturated and polyunsaturated fats are plentiful in our food system.

% adipose

dietary

adipose / dietary

saturated

30%

36%

81%

monounsaturated

54%

42%

129%

polyunsaturated

16%

22%

75%

The chart below shows the relative proportions of each of the fatty acids in human adipose tissue.  Oleic acid (18:1) (a monounsaturated fat) is the most plentiful, followed by Palmitic acid (16:0) (a saturated fat) and Linoleic acid (18:2) (a polyunsaturated fat).image004

Taking Volek and Phinney’s logic a step further, the table below shows a comparison of the proportion of each fatty acid in our adipose tissue compared to their availability in the modern diet (based on the average across the 8000 foods in the USDA database).  It appears that we have more than enough Stearic acid (18:0), Linoleic acid (18:2) and Linolenic acid (18:3) available in the food system while a number of the other fatty acids are deficient.

isomer

adipose (mol %) % adipose dietary adipose / dietary class

14:0

2.8

3.0% 2.7% 110%

SFA

16:0

21.5

23.0% 17.4% 132%

SFA

16:1 n-7

7.2 7.7% 2.08% 369%

MUFA

18:0

3.4 3.6% 9.2% 39%

SFA

18:1 n-9

43.5 46.5% 36.6% 127%

MUFA

18:2 n-6

13.9 14.9% 17.5% 85%

PUFA

18:3 n-3

0.8 0.9% 1.8% 48%

PUFA

20:3 n-6

0.2 0.2% 0.012% 1744%

PUFA

22:4 n-6

0.1 0.1% 0.004% 2426%

PUFA

22:5 n-3

0.1 0.1% 0.1% 140%

PUFA

22:6 n-3 0.1 0.1% 0.3% 37%

PUFA

oleic acid versus linoleic acid

The two most prevalent fats in our diet and on our body are Oleic acid (18:1) and Linoleic acid (18:2).

While Linoleic acid (18:2) is considered to be an essential fatty acid [14] (meaning that the body cannot manufacture it from other dietary components) the data in the table above indicates that there is a relative abundance of it in the dietary system.

Many people believe that excess Linoleic acid (18:2) from vegetable oils (which causes an imbalance in our omega 3 : omega 6 ratio) is a major contributor to the obesity epidemic. [15]

The common wisdom is that olive oil, which is high in the monounsaturated fat Oleic acid (18:1), is a healthy ‘good fat’. [16]  When we look at the research it appears well established that emphasising the monounsaturated Oleic acid (18:1) and reducing the polyunsaturated Linoleic acid (18:2) will improved insulin resistance.[17] [18] [19] [20]

omega 3 fatty acids

Improving the omega-3 : omega-6 ratio is widely regarded as important to reduce inflammation and optimise brain function and mental health.[21] [22]    Omega 3 fatty acids are typically obtained from seafood and are generally considered to be ‘good fats’ that we should be maximising for health.

While there appears to be plenty of DHA (22:6 n-3) available in the diet when we simply consider the composition of adipose tissue, it’s worth noting that DHA makes up 30% of the brain and 50% of our retina, so it is probably going to fall into the category of ‘good fats’ that we should be going out of our way to pursue in our diet.

A recent mouse study showed that fish oil (high in omega 3 fatty acids) is better than lard (high in saturated fatty acids, particularly palmitic acid (16:0) and stearic acid (18:0)) when it comes to weight gain, gut bacteria, obesity and insulin resistance.[23]  While people are clearly different from mice, it’s not unreasonable to think that fish oil might be better than eating lard.

Omega 3 fats are relatively rare in our food system which means we need to go out of our way to incorporate them into our diet.   The table below shows the omega 3 fatty acids that I think we should count as good fat along with the foods they are commonly found in.

isomer common name common foods
22:6 n-3 (DHA) Docosahexaenoic acid (DHA) fish oil, caviar, seal oil, cod liver oil, sardine oil
20:5 n-3 (EPA) Eicosapentaenoic acid (EPA) fish oil, caviar, fish
18:3 n-3 c,c,c (ALA) Alpha-linolenic acid peanut butter, flax seed, butter
22:5 n-3 (DPA) Docosapentaenoic acid (DPA) seal oil, fish oil – menhaden, fish oil – salmon.

MCT oils

You might have heard a lot of talk about MCT (medium chain triglycerides) oils recently.  These shorter chain fats appear to bypass the lymphatic system and are transported directly to the liver via the portal vein.

Many people find benefit from using MCT oil as an aid to extend periods between meals or and cognitive enhancement.[24]  MCT oils are more readily turned into ketones which provide an alternative fuel source to the brain.   In turn, ketones can increase satiety[25] and decrease appetite, both of which may facilitate weight loss.[26]

image005

MCTs make up about 1.1% of the fats in our food supply in coconut oil, butter, cheese and cream, however to get higher levels you will to supplement.

isomer common name common foods
12:0 Lauric acid palm kernel oil, coconut oil
10:0 Capric acid cheese, coconut oil, palm kernel oil
8:0 Caprylic acid coconut oil, coconut cream, palm kernel oil
6:0 Caproic acid butter, cheese, cream

trans fats

Artificial trans fats (a.k.a. partially hydrogenated oils) are one of the few components of the diet that are widely accepted as unhealthy.[27]   If you look at the foods in which artificial trans fats are the most prevalent, it’s hard to disagree.

isomer common foods
18:1 t (g) soy shortening, margarine, canola oil
18:2 t (g) KFC, margarine
18:2 t,t (g) McDonald’s, fast foods
16:1 t (g) thickshake, cheeseburger, hamburger, fast foods

The issue with counting all trans fats as a bad fat is that they can also occur naturally in small amounts in meats and dairy such as grass fed beef.[28] [29]

image006

Given that the USDA database does not differentiate between partially hydrogenated oils and naturally occurring trans fats, I have not assigned trans fats a negative mark.  Emphasising other ‘good fats’ will demote foods that contain artificial trans fats.

the effect of replacing carbohydrates with fat

The common view is that dietary fat, particularly saturated and trans fats, should be avoided in order to optimise blood cholesterol markers.  But what happens when we substitute fat for carbohydrates?

The chart below from a paper by cardiologist Dariush Mozaffarian[30] indicates that trans fats (TFA) have a negative impact on all blood markers (i.e. TC/HDL, LDL and HDL).  So there’s no disagreement there.

However increasing dietary saturated fat:

  • increases LDL (note: this is generally considered to be bad although it’s not clear if this is large buoyant of small dense LDL),
  • has minimal effect on the total cholesterol to HDL ratio, and
  • increases HDL (good).

Replacing carbohydrates (CHO) with either monounsaturated (MUFA) or polyunsaturated (PUFA) have what are generally regarded to be positive outcomes.

image007

Whether or not saturated fat is beneficial starts to become a little clearer when we look at the effect of individual fatty acids.  The data below shows that while Lauric acid (12:0) increases LDL it also has very a positive effect on increasing HDL and decreasing the TC : HDL ratio.

image008

saturated fats and insulin resistance

Mozaffarian says

“SFA has been considered a risk factor for insulin resistance and diabetes mellitus, but review of the current evidence indicates surprisingly equivocal findings. SFA consumption inconsistently affects insulin resistance in controlled trials and has not been associated with incident diabetes in prospective cohort studies.”[31]

image009

Things start to get more interesting when you look at the relationship between individual fatty acids, insulin resistance and type 2 diabetes.

The investigators found that saturated fatty acids with an odd number of carbon atoms in their chain (15:0 and 17:0) were associated with a lower risk of type 2 diabetes, whereas even-chain saturated fatty acids—14:0, 16:0, and 18:0—were associated with a higher risk.  Longer-chain saturated fatty acids (20:0, 22:0 and 24:0) also were found to be inversely associated with incident type 2 diabetes. [32] [33] [34]   

This also aligns with the mouse study that mentioned above where fish oil was found to have a better outcome on obesity and gut health compared to lard (which is high in 16:0 and 18:0).

image010

The table below shows the foods that these ‘good fats’ are contained in.  Meat and nuts are embraced in the paleo and low carb scenes.  The benefits of dairy are debated, but this is typically related to the casein and lactose content which some people don’t tolerate well.

isomer common name common foods
17:0 Heptadecanoic acid tofu, lamb, beef
20:0 Arachidic acid macadamia nuts, peanut butter
22:0 Behenic acid peanut oil, peanut butter, sunflower oil, macadamia nuts
15:0 Pentadecanoic acid cream cheese, sour cream, lamb, beef
24:0 Lignoceric acid peanut butter, rosemary, macadamia nuts, cashew nuts, sunflower seeds

summary

Listed below (in order of prevalence in the dietary system) are the ten fatty acids that I think should be included in the list of ‘good fats’ along with the common foods that they are contained in and the basis for their inclusion.

fatty acid common foods comment
Oleic acid (18:1) olive oil, sunflower oil, hazelnut oil, safflower oil, soybean oil, almond oil, avocado oil commonly associated with positive health outcomes and key component of Mediterranean diet

improves insulin resistance.

most abundant fatty acid in human adipose tissue

underrepresented in food system.

reduces TC:HDL ratio

Lauric acid (12:0) palm kernel oil, coconut oil increases HDL

decreases TC:HDL ratio.

Alpha-linolenic acid (18:3 n-3) peanut butter, flaxseed, nuts, cloves, cheese omega-3.

inflammation lowering

improves insulin resistance

Capric acid (10:0) cheese, coconut oil MCT oil.

Improves HDL:LDL ratio.

Docosahexaenoic acid (DHA) (22:6 n-3) fish oil – salmon, caviar, seal oil, cod liver oil, sardine oil essential fatty acid

omega 3.

abundant in human brain.

Arachidonic acid (20:4) salmon, chicken heart, liver, brain conditionally essential.

rare in food system.

Eicosapentaenoic acid (EPA) (20:5 n-3) fish oil, caviar, fish omega-3.

inflammation lowering.

improves brain function.

Margaric acid (17:0) tofu, lamb, frankfurter, beef sausage reduced risk of type 2 diabetes.
Docosapentaenoic acid (DPA) (22:5 n-3) seal oil, fish oil – menhaden, fish oil – salmon omega-3 though small quantities.
Pentadecanoic acid (15:0) cream cheese, sour cream, lamb. lower risk of type 2 diabetes

And for completeness listed below (in order of their prevalence in the dietary system) are the fatty acids in the USDA food database that didn’t make the ‘good fats’ list.

fatty acid common foods comment
Linoleic acid (18:2) safflower oil, grapeseed oil, sunflower oil, walnut oil n-6 component is essential however overly abundant in food system

substituting linoleic acid for oleic acid has been shown to improve insulin resistance

Palmitic acid (16:0) palm oil, fish oil – menhaden, butter, lard higher risk of type 2 diabetes

poor gut bacteria outcomes in mice study

Stearic acid (18:0) cocoa butter, shortening, margarine, lard increased risk of type 2 diabetes.

poor gut bacteria outcomes in mice study.

overly abundant in food system

18:1 c canola oil, margarine subset of 18:1 – no need to double count
18:2 n-6 c,c soy oil, sunflower oil, soybean oil, mayonnaise subset of 18:2.
Myristic acid (14:0) nutmeg, coconut oil Increased risk of type 2 diabetes
Palmitoleic acid (16:1) macadamia nuts, fish oil, seal, whale Increased risk of type 2 diabetes
Linolenic acid (18:3) flax seed, chia seed, walnuts, basil adequate in food system.

only count n-3 ALA component.

18:1 t Soy shortening, margarine, canola oil. trans fat
Gadoleic acid (20:0) seal, eel, fish oil – herring, fish -–halibut, fish oil – cod liver, salmon small quantities and limited research.
Caprylic acid (8:0) coconut oil, coconut cream. MCT but rare in food system other than manufactured foods
Erucic acid (22:1) herring, halibut, sardine, cod liver no clear health benefits / research
Butyric acid (4:0) butter, cheese MCT but rare in food system other than manufactured foods
16:1 c KFC, Popeye’s, fast food predominantly in fast foods.
Caproic acid (6:0) butter, cheese, cream. MCT but rare in food system other than manufactured foods
Arachidic acid (20:0) macadamia nuts, peanut butter. reduced risk of type 2 diabetes but rare in food system.
Behenic acid (22:0) peanut oil, peanut butter, sunflower oil, macadamia  nuts, reduced risk of type 2 diabetes but rare in food system.
Myristoleic acid (14:0) frankfurter, beef sausage, bologna, cream cheese minimal research.

small quantities in food system

18:2 i soy oil, canola oil, margarine, French fries minimal research.

small quantities in food system

Heptadecenoic acid (17:0) tofu, broccoli, beef minimal research.

small quantities in food system

18:2 t KFC, margarine trans fat
18:4 fish oil – sardine, fish oil – salmon, fish oil – menhaden, oysters very small quantities in food system
Eicosadienoic acid (20:2 n-6 c,c) English muffin, margarine, fast foods, pine nuts, ham
Lignoceric acid (24:0) peanut butter, rosemary, macadamia nuts, cashew nuts, sunflower seeds reduced risk of type 2 diabetes
18:2 t,t MacDonald’s, fast foods trans fat
Eicosatrienoic acid (20:3) pine nuts, mustard, whitefish, seal, salmon appears beneficial but minimal quantities in food system
Pentadecenoic acid (15:0) tofu, miso, beef sausage appears beneficial but minimal quantities in food system
Gamma-linolenic acid (18:3 n-6) margarine omega 6

minimal quantities.

16:1 t thick shake, cheeseburger, hamburger, fast foods. trans fat
20:3 n-6 KFC, Popeye’s, fast food. Omega 6 and primarily in fast food
Nervonic acid (24:1 c) mustard, salmon, seal, flax seed likely beneficial, but minimal quantities
22:1 c margarine. minimal quantities in food system

optimal fatty foods

Shown below is the list of fatty foods sorted by their relative quantity of the good fats with their percentage of insulinogenic calories also shown.  The order itself is not that important (otherwise the seals and whales would be even more endangered due to this article), however the big winners are:

  • fish oil (seal, whale, menhaden, sardine, herring, salmon, cod liver),
  • fish (smelt, salmon, herring, caviar, mackerel, caviar, trout, swordfish),
  • lamb, pork and beef, and
  • cheese, butter and cream.
food % insulinogenic nutrient density
oil – bearded seal 0% 20.6
oil – beluga whale 0% 17.9
oil – spotted seal 0% 17.4
smelt – dried 33% 14.4
salmon 39% 14.1
fish oil – cod liver 0% 14.0
fish oil – salmon 0% 13.4
fish oil – sardine 0% 13.1
fish oil – menhaden 0% 13.0
fish oil – herring 0% 12.7
lamb fat 2% 12.7
mackerel 14% 11.5
pork fat 3% 11.0
whitefish 38% 10.9
cream cheese 8% 10.4
caviar 26% 10.3
bacon fat 0% 9.8
butter 0% 9.0
roe 37% 8.9
sablefish 16% 8.7
seal 22% 8.5
beef steak 21% 8.3
parmesan cheese 24% 8.2
herring 19% 8.2
whitefish 33% 8.2
pepperoni 10% 8.1
beef sausage 9% 7.5
turkey fat 0% 7.1
lamb 16% 7.1
macadamia nuts 5% 7.0

It’s important to keep in mind that consuming enough “good fats” is only part of the nutrition story.  In the next article we’ll look at how we can use this understanding of good fats along with our understanding of vitamins, mineral and amino acids to identify the most nutrient dense foods for different goals.

references

[1] https://optimisingnutrition.wordpress.com/2015/03/22/diabetes-102/

[2] https://optimisingnutrition.wordpress.com/2015/03/23/most-ketogenic-diet-foods/

[3] http://www.mayoclinic.org/healthy-lifestyle/nutrition-and-healthy-eating/in-depth/fat/art-20045550?pg=2

[4] http://health.usnews.com/best-diet/mediterranean-diet

[5] http://diabeticmediterraneandiet.com/ketogenic-mediterranean-diet/

[6] http://www.mayoclinic.org/healthy-lifestyle/nutrition-and-healthy-eating/in-depth/mediterranean-diet/art-20047801

[7]  http://www.nature.com/ejcn/journal/v56/n10/full/1601413a.html

[8] http://www.internationaloliveoil.org/estaticos/view/87-mediterranean-diet-pyramid

[9] http://www.ncbi.nlm.nih.gov/pubmed/10700478

[10] http://ajcn.nutrition.org/content/61/6/1402S.full.pdf+html

[11] http://www.artandscienceoflowcarb.com/

[12] http://www.amazon.com/The-Art-Science-Carbohydrate-Performance/dp/0983490716

[13] http://www.researchgate.net/publication/5416860_Hodson_L_Skeaff_CM_Fielding_BA._Fatty_acid_composition_of_adipose_tissue_and_blood_in_humans_and_its_use_as_a_biomarker_of_dietary_intake._Prog_Lipid_Res_47_348-380

[14] https://en.wikipedia.org/wiki/Linoleic_acid

[15] http://www.forbes.com/sites/realspin/2015/09/29/could-so-called-healthy-vegetable-and-seed-oils-be-making-us-fat-and-sick/

[16] http://www.mayoclinic.org/healthy-lifestyle/nutrition-and-healthy-eating/in-depth/mediterranean-diet/art-20047801

[17] http://www.ncbi.nlm.nih.gov/pubmed/10700478

[18] http://www.ncbi.nlm.nih.gov/pubmed/14713277

[19] http://qjmed.oxfordjournals.org/content/93/2/85

[20] http://www.ncbi.nlm.nih.gov/pubmed/10700478

[21] http://www.ncbi.nlm.nih.gov/pubmed/12442909

[22] http://chriskresser.com/how-too-much-omega-6-and-not-enough-omega-3-is-making-us-sick/

[23] http://www.the-scientist.com/?articles.view/articleNo/43854/title/how-fats-influence-the-microbiome/

[24] http://www.bulletproofexec.com/how-to-make-your-coffee-bulletproof-and-your-morning-too/

[25] http://www.nature.com/ijo/journal/v25/n9/full/0801682a.html

[26] http://www.nature.com/ijo/journal/v25/n9/full/0801682a.html

[27] http://www.marksdailyapple.com/why-are-trans-fats-bad/#axzz3mSg8Rg6D

[28] http://chriskresser.com/can-some-trans-fats-be-healthy/

[29] http://www.ncbi.nlm.nih.gov/pubmed/21427742

[30] http://www.ncbi.nlm.nih.gov/pubmed/20354806

[31] http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2950931/

[32] http://www.thelancet.com/journals/landia/article/PIIS2213-8587(14)70166-4/fulltext?rss=yes

[33] http://www.medscape.com/viewarticle/829920

[34] http://www.thelancet.com/action/showFullTextImages?pii=S2213-8587%2814%2970146-9