When Fat Became the Villain

Those who are younger than 40 years old probably grew up hearing that saturated fat is “bad” and polyunsaturated fat is “good”, but where did we get this idea and is it true?

The process of what I call the “vilification of fat” began when researcher Ancel Keys presented a graph at a talk at Mount Sinai Hospital in New York in January 1953 and later published it in a research paper titled Atherosclerosis: a problem in newer public health [1]. It was said to show the relationship between ‘fat calories as a percentage of total fat” and the number of ‘deaths from degenerative heart disease per 100,000 people’ for men between the ages of 45-49 and 55-59. The linear relationship of these data points from the Six Country Study (Japan, Italy, England & Wales, Australia, Canada and the USA) suggested that there was a strong relationship between the amount of fat calories as a percentage of dietary intake and deaths from degenerative heart disease for men aged 55-59. At the time of publication of the Six Country Study, Keys said that it was possible to only get complete data from those 6 countries [1] at the time. He concluded;

“Whether or not cholesterol etc. are involved, it must be concluded that dietary fat somehow is associated with cardiac diseases mortality, at least in middle age [1].

In Key’s mind, the total amount of dietary fat was “somehow associated” with cardiac death in middle aged men, but he expressed doubt whether or not cholesterol was involved.

In 1957, Yerushalamy and Hilleboe [2] published data from 22 countries which showed there was no linear relationship between ‘fat calories as a percentage of total fat” and the number of ‘deaths from degenerative heart disease per 100,000 people’.

Keys went onto conduct what became known as the Seven Country Study which collected data on almost 13,000 men aged 40-59 from the USA, Finland, the Netherlands, Yugoslavia, Greece and Japan. Findings were only published in 1970 in the journal Circulation in several papers from separate countries [3]. Keys no longer believed that total fat was associated with heart disease but that saturated fat was the villain. Keys concluded that the average consumption of animal foods (with the exception of fish) was positively associated with 25-year heart disease death rates and that the average intake of saturated fat was strongly related to 10 and 25-year coronary heart disease death rates.

What solidified this association was that the 1970 publication on the Seven Country Study contained Keys’ 1953 graph from the Six Country Study (above) [4]. Even though it indicated a linear relationship between total fat intake and degenerative heart disease it became tied in the minds of many that this graph “proved” that saturated fat was linked to heart disease—even though that is not what the graph shows at all.  It isn’t even about saturated fat. Keys also neglected to mention Yerushalamy and Hilleboe’s data from 22 countries showed no relationship between total fat consumption and heart disease.

The Diet Heart Hypothesis

The diet-heart hypothesis originated with Ancel Keys and is the belief that eating foods high in saturated fat contributes to heart disease. Keys believed that replacing fat from meat, butter and eggs with newly-created polyunsaturated vegetable oils such as soybean oil would reduce heart disease and deaths by lowering blood cholesterol levels.

The Sugar Industry Funding of Research Vilifying Fat

In the mid-1960’s, the Sugar Research Foundation (predecessor of the Sugar Association) wanted to offset research that had been published and that suggested that sugar was a more important a cause of heart disease and stroke from atherosclerosis than dietary fat. The Sugar Research Foundation invited Dr. Fredrick Stare and the late Dr. D. Mark Hegsted of Harvard’s School of Public Health Nutrition Department to join its scientific advisory board and then approved $6,500 in funds ($50,000 in 2016 dollars) to support a review article that would respond to the research showing the danger of sucrose [5]. Letters exchanged between the parties came to light a November 2016 article published by Kearns et al [6] which said that the Sugar Research Foundation had tasked the Harvard researchers with preparing “a review article of the several papers which find some special metabolic peril in sucrose and, in particular, fructose [7]”.

The Sugar Industry paying researchers to blame dietary fat and vindicate sugar for heart disease seems a little like the tobacco industry having secretly funded articles demonstrating that something other than smoking was responsible for lung cancer.

In August 1967 the New England Journal of Medicine published the first review article written by Drs. Stare, Hegsted and McGandy titled “Dietary fats, carbohydrates and atherosclerotic vascular disease” which stated;

Since diets low in fat and high in sugar are rarely taken, we conclude that the practical significance of differences in dietary carbohydrate is minimal in comparison to those related to dietary fat and cholesterol”.

The report concluded;

the major evidence today suggests only one avenue by which diet may affect the development and progression of atherosclerosis. This is by influencing the levels of serum lipids [fats], especially serum cholesterol.”

The Harvard researchers went on to say;

there can be no doubt that levels of serum cholesterol can be substantially modified by manipulation of the fat and cholesterol of the diet” and that “on the basis of epidemiological, experimental and clinical evidence, that a lowering of the proportion of dietary saturated fatty acids, increasing the proportion of polyunsaturated acids and reducing the level of dietary cholesterol are the dietary changes most likely to be of benefit.

At no point did Stare, Hegsted and McGandy disclose that they were paid by the Sugar Research Foundation for the two-part review.

A commentary in the Journal of Accountability in Research [8] summarized the significance of those articles as follows;

“Researchers were paid handsomely to critique studies that found sucrose [sugar] makes an inordinate contribution to fat metabolism and heart disease leaving only the theory that dietary fat and cholesterol was the primary contributor.”

The same Dr. Hegsted that was funded by the Sugar Industry to write the above articles vindicating sugar and vilifying dietary fat went on to work on editing the 1977 US Dietary Guidelines [9], which entrenched the vilification of fat into the US Food Pyramid for the next 40+ years. The rest, they say, is history.

The same year (1977), Canada’s Food Guide recommended that Canadians limit fat to <30% of daily calories with no more than 1/3 from saturated fat but did not specify an upper limit for dietary cholesterol. This was based on the belief that total dietary fat and saturated fat were responsible blood levels of LDL cholesterol levels and total serum cholesterol [10]. Cholesterol in general (total cholesterol) and LDL cholesterol was assumed to be tied to heart disease, so the focus was on lowering the proxy measurements of LDL cholesterol and total cholesterol.

Recommendations for the continued restriction of dietary fat continued in both the US and Canada in the 2015 revision of the Dietary Guidelines based on the enduring belief that lowering saturated fat in the diet would lower blood cholesterol levels and reduce heart disease.

The question is does it?

A 2018 study published in the journal Nutrients looked at health and nutrition data from 158 countries from 1993-2011 and found that total fat and animal fat consumption were least associated with the risk of cardiovascular disease and that high carbohydrate consumption,  particularly as cereals and wheat was most associated with the risk of cardiovascular disease [11]. Significantly, both of these relationships held up regardless of a nation’s average national income.

These findings support those of the 2017 PURE (Prospective Urban and Rural Epidemiological) study, the largest-ever epidemiological study which recorded dietary intake of 135,000 people in 18 countries over an average of 7 1/2 years, including high-, medium- and low-income nations. The PURE study found an association between raised cholesterol and lower  cardiovascular risk and that “higher carbohydrate intake was associated with higher risk of total mortality”. It also reported that “total fat and individual types of fat were related to lower total mortality (death)” [12].

A recent study published in the American Journal of Clinical Nutrition reports that long-term consumption of the saturated fat found in full-fat dairy products is not associated with an increased risk of cardiovascular disease (atherosclerosis, coronary artery disease, etc.) or other causes of death, and may actually be protective against heart attack and stroke [13].

This recent large-scale epidemiological data provides strong evidence that eating a diet containing saturated fat is not associated with heart disease. While eating saturated fat raises blood levels of LDL cholesterol, we now know that there is more than one type of LDL cholesterol and only the small, dense LDL cholesterol is linked to atherosclerosis. The large, fluffy LDL is protective [14].

We now know that fat was made out to be the villain in scientific reviews paid for by the sugar industry and this combined with Ancel Key’s Diet-Heart Hypothesis ended up being the impetus for the creation of an entire food industry designed to extract fat from industrial seed oils, such as soybean oil and rapeseed (Canola). These industrial seed oils are the so-called “healthy polyunsaturated fats” that we are encouraged to eat instead of so-called “dangerous” saturated fat, yet these industrial seed oils are only able to be produced using solvent-based chemical extraction under very high temperature. Should we be confident in industrial fats brought to us by the same industry that brought us “trans fats”? With a lack of evidence that natural fats such as butter or cream are dangerous, perhaps eating a bit of real animal fat and plenty of natural plant-based monounsaturated fats such as olive oil is the better way to go?

For more than forty years, generations of Americans and Canadians have avoided eggs, full fat cheese and creamery butter – and done so because they have believed that saturated fat raising LDL cholesterol predisposed them to heart disease. We know much more than we did in the 1970s when the first Dietary Guidelines were created in the US (under the watchful editorial oversight of one of the researchers that had been paid by the sugar industry to vilify fat).  We now know that eating foods with saturated fat will raise LDL-cholesterol, but not all LDL-cholesterol is “bad”[14]. Before we knew this high total LDL-cholesterol (LDL-C) was seen as a good proxy (indirect substitute) measurement for heart disease risk, but no longer.

It has been known since the early 1990s that a high TG:HDL ratio is very good estimator of coronary heart disease risk [15].

The measurement of the LDL-cholesterol particle number (LDL-P) which measures the actual number of LDL particles is a much stronger predictor of cardiovascular events than LDL-C [16] because the more particles there are, the more small, dense LDL there are.

The ratio of apolipoprotein B (apoB): apolipoprotein A (apoA) is another good estimator of cardiovascular risk. Lipoproteins are particles that transport cholesterol and triglycerides (TG) in the blood stream and are made up of apolipoproteins, phospholipids, triglycerides and cholesterol. Apolipoprotein B is an important component of many of the lipoprotein particles associated with atherosclerosis, such as chylomicrons, VLDL, IDL, LDL – with most found in LDL. Since each lipoprotein particle contains one apoB molecule, measuring apoB enables the determination of the number of lipoprotein particles that contribute to atherosclerosis and for this reason that ApoB is considered a much better predictor of cardiovascular disease risk than LDL-C [17].

In light of the recently published epidemiological evidence and much stronger proxy measurement of cardiovascular risk we must update our thinking that fat in general, or saturated fat in particular is the “villain”. It’s not.

Perhaps you could use some help as to which fats you should eat more of and in what amounts, or on deciding on what ratio of protein to fat in your diet will best help you reach your health and weight goals? I can help.

I provide services via Distance Consultation (Skype, long distance telephone) as well as in-person in my Coquitlam office.

If you have questions on my services, please send me a note using the Contact Me form located on the tab above, and I will reply as soon as I’m able.

To our good health!


If you would like to read well-researched, credible “Science Made Simple”  articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please  click here.

You can follow me at:



Copyright ©2018  The LCHF-Dietitian (a division of BetterByDesign Nutrition Ltd.) 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.


  1. Keys, A., Atherosclerosis: a problem in newer public health. J Mt Sinai Hosp N Y, 1953. 20(2): p. 118-39.
  2. Yerushalamy, J. and Hilleboe HE, Fat in the diet and mortality from heart disease; a methodologic note. N Y State J Med, 1957. 57(14): p. 2343-54.
  3. Coronary heart disease in seven countries. Summary. Circulation, 1970. 41(4 Suppl): p. I186-95.
  4. Harcombe, Z., An examination of the randomised controlled trial and epidemiological evidence for the introduction of dietary fat recommendations in 1977 and 1983:  A systematic review and meta-analysis. 2015, University of the West of Scotland.
  5. Husten, L., How Sweet: Sugar Industry Made Fat the Villain. 2016.
  6. Kearns, C.E., L.A. Schmidt, and S.A. Glantz, Sugar Industry and Coronary Heart Disease Research: A Historical Analysis of Internal Industry Documents. JAMA Intern Med, 2016. 176(11): p. 1680-1685.
  7. McGandy, R.B., D.M. Hegsted, and F.J. Stare, Dietary fats, carbohydrates and atherosclerotic vascular disease. N Engl J Med, 1967. 277(4): p. 186-92 contd.
  8. Krimsky, S., Sugar Industry Science and Heart Disease. Account Res, 2017. 24(2): p. 124-125.
  9. Hegsted D.M. Introduction to the Dietary Goals for the United States. p. 17 of 130.
  10. McDonald, B.E., The Canadian experience: why Canada decided against an upper limit for cholesterol. J Am Coll Nutr, 2004. 23(6 Suppl): p. 616S-620S.
  11. Grasgruber, P., et al., Global Correlates of Cardiovascular Risk: A Comparison of 158 Countries. Nutrients, 2018. 10(4).
  12. Dehghan, M., et al., Associations of fats and carbohydrate intake with cardiovascular disease and mortality in 18 countries from five continents (PURE): a prospective cohort study. Lancet, 2017. 390(10107): p. 2050-2062.
  13. de Oliveira Otto, M.C., et al., Serial measures of circulating biomarkers of dairy fat and total and cause-specific mortality in older adults: the Cardiovascular Health Study. Am J Clin Nutr, 2018.
  14. Lamarche, B., I. Lemieux, and J.P. Després, The small, dense LDL phenotype and the risk of coronary heart disease: epidemiology, patho-physiology and therapeutic aspects. Diabetes Metab, 1999. 25(3): p. 199-211.
  15. Manninen, V., et al., Joint effects of serum triglyceride and LDL cholesterol and HDL cholesterol concentrations on coronary heart disease risk in the Helsinki Heart Study. Implications for treatment. Circulation, 1992. 85(1): p. 37-45.
  16. Cromwell, W.C., et al., LDL Particle Number and Risk of Future Cardiovascular Disease in the Framingham Offspring Study – Implications for LDL Management. J Clin Lipidol, 2007. 1(6): p. 583-92.
  17. Lamarche, B., et al., Apolipoprotein A-I and B levels and the risk of ischemic heart disease during a five-year follow-up of men in the Québec cardiovascular study. Circulation, 1996. 94(3): p. 273-8.



Homemade Olive Oil Mayonnaise

This recipe is posted as a courtesy to those following a variety of low-carb and ketogenic diets (not necessarily Meal Plans designed by me). This recipe may or may not be appropriate for you.

Many people buy ‘olive oil mayonnaise‘ without realizing it is only canola oil mayonnaise with added olive oil. The first ingredient is canola oil.  This popular brand reads “made with” in fine print.

So much for people’s good intentions of substituting a healthy monounsaturated fat for a refined, industrial seed oil like canola.

I’ve been wanting to make my own mayo for a while, but my concern was using raw egg due to the risk of salmonella contamination.

Then I found out that pasteurized eggs are available for purchase in the US although I have been unable to find them here, but there are instructions online for how to do it yourself. It’s super easy.  All you need is an accurate thermometer and a few minutes of time.

Today, I pasteurized a dozen eggs and then made real mayonnaise.

There are only two things to keep in mind to be successful.  Be sure to have all your ingredients at room temperature before you begin and use “light” or “light-tasting” olive oil.  There are several brands, including in-house brands of this that come from Italy.  While I love cold-pressed extra virgin olive oil on everything else, I’ve read in multiple places and been told by a girlfriend that makes her own mayonnaise that the result is too heavy and bitter if made with cold pressed oil.

This one is just perfect!


1/4 cup light olive oil
1 cup light olive oil
1 large egg, pasteurized
1/2 teaspoon Keen’s hot mustard
1/2 teaspoon salt
1/2 tsp white vinegar
1/2 lemon, juiced


1 -Place the egg, mustard and salt in a tall, thin metal pitcher and stir in only 1/4 cup of olive oil. Mix thoroughly.

2 -Insert a stick blender and turn it on high, then very slowly drizzle in the remaining cup of olive oil.

Note: don't rush this part, because adding the olive oil too fast will result in the mixture separating.

3 -After all the oil has been added and the mixture is emulsified, add the vinegar, lemon juice and stir gently with a spoon to blend.

4 – Store the mixture in the refrigerator in an airtight container.


If you would like to read well-researched, credible “Science Made Simple”  articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please  click here.

You can follow me at:



Note: This is the link that I used for pasteurizing eggs. I calibrated a new thermometer with boiling water (100° C) to be sure temperature readings were accurate and would encourage you to do the same. Temperature accuracy is critical here, as is time. Please read their disclaimer at the bottom and their note for pregnant women avoid raw eggs.

How Much and Which Types of Fat?

I often get asked ‘how much fat should people on a low carb high fat diet eat’ and ‘which types of fat’? In this article I answer both questions.

As mentioned in previous blogs, there are many types of “low carb diets” -ranging from moderately low carb diets (~130 g carbs) such as the one the American Diabetes Association recommends for weight loss in those with Type 2 Diabetes, to ketogenic low carb diets (5-10% net carbs), and everything in between.

In any low carb diet, carbs (5-10% net carbs) are supplied in foods such as non-starchy vegetables, nuts and seeds, and certain fruit.

In a moderately low carb diet, ~25% of calories come from carbs found in the same foods as with a keto low carb diet, along with the addition of milk and yogurt, legumes, and small amounts of grain products.

What low carb diets have in common is that they provide adequate but not excess protein (~75-120 gms total protein), varying amounts of  carbs  (35-40 gm in a ketogenic diet, 130 gm in a moderately low carb diet), with the remaining calories coming from healthy fats.

What kinds of fat?

Some types of low carb diets (e.g. Paleo diets, Dr. Atkins diet, etc.) include large amounts of red meat, including processed meat such as bacon and sausage, and an abundance of cream and butter. While there is nothing inherently ‘bad’ about saturated fat for healthy people (covered in a previous article), there are some individuals with specific risk factors or disease conditions that might benefit by taking a more conservative approach with regards to the total amount they eat of these types of fats.

Unless required for clinical reasons, the low carb diets I teach include the saturated fat found naturally in the protein foods for the day, as well as butter for cooking or seasoning vegetables, mayo for canned fish or eggs,  and a dollop of sour cream with a meal or cream in coffee. If, for example people love the crispy skin on a barbecued chicken and there is no compelling reason to remove it, then they can by all means enjoy it. Same for the visible fat around the outside of a rib steak.

That said, I see no justifiable reason for adding “fat bombs” to the diet or drinking “bullet proof coffee” made with added butter and coconut oil – especially for individuals who have been overweight or obese and have leptin resistance (covered in an earlier article), that accompanies insulin resistance.

Most of the fats that I recommend people eating should be a natural part of  meals and come from mono-unsaturated fruits, such as avocado and olives, from a wide variety of nuts and seeds (as well as from the oils from these foods), from coconut oil used for cooking, as well as from omega 3 fats found abundantly in certain kinds of fish, such as salmon, mackerel and tuna.

It is important to keep in mind as covered in earlier articles, that if one is limiting carbohydrates then sufficient fat is required from which the body will make ketones for fuel, as well as for one of the sources (along with protein) from which it can synthesize the small amount of glucose (130 g / day) that it needs for brain function. Of course, when a person is completely fasting (religious reasons, medically supervised, etc.) the 130 g / day of glucose needed by the brain can be made from fat stores.

Remember too, that when limiting carbohydrates, eating adequate amounts of healthy fat along with sufficient protein will keep you from getting hungry between meals by increasing satiety (the feeling of ‘fullness’ that fat provides), so when you are planning your meals, be sure to include a variety of types of fat in sufficient quantity.

If you are following a low carb high fat approach, feel free to add olives on top of a Greek salad and drizzle it with a beautiful extra virgin olive oil.

Enjoy homemade guacamole with blackened fish or a salad sprinkled with nuts or seeds and topped with a macadamia nut balsamic vinaigrette.  These are just some of the delicious ways to enjoy added fat.

Want to know which kind of low carb high fat diet might be best for you?

Please send me a note using the “Contact Me” form on this web site.

To our good health!


If you would like to read well-researched, credible “Science Made Simple”  articles on the use of a low carb or ketogenic diet for weight loss, as well as to significantly improve and even reverse the symptoms of Type 2 Diabetes, high cholesterol and other metabolic-related symptoms, please  click here.

You can follow me at:



Note: There is no one-size-fits-all approach to following a Low Carb High Fat lifestyle since everybody's nutritional needs and health status is different. If you want to adopt this kind of lifestyle, please discuss it with your doctor.

Copyright ©2018 – The Low Carb High Fat Dietitian (a division of BetterByDesign Nutrition Ltd.) 

LEGAL NOTICE: The contents of this blog, including text, images and cited statistics as well as all other material contained here (the “content”) are for information purposes only.  The content is not intended to be a substitute for professional advice, medical diagnosis and/or treatment and is not suitable for self-administration without the knowledge of your physician and regular monitoring by your physician. Do not disregard medical advice and always consult your physician with any questions you may have regarding a medical condition or before implementing anything  you have read or heard in our content.





The “Skinny” on Fats


Many people believe that saturated fat is “bad” for you but few people realize that our bodies actually manufacture it.  It’s true. In this article, I cover “just enough” chemistry (made very easy!!) for you to be able to understand the latest new findings. My next article will be on a change in the dietary recommendations of a key stakeholder in heart health in Canada, and what this change means.

If Saturated Fat was so Dangerous, Why Would our Body Actually Make it? 

There are two sources of fats (also called “lipids“); those we eat in our diets and those our body makes. The fats we eat are called “exogenous fats” (“exo” meaning ‘from outside’) and the type of fats that our body makes are called “endogenous fats” (“endo” meaning ‘from within’).

Exogenous Fats

The types of fat that our body takes in as exogenous lipids from what we eat include saturated fats, and different kinds of unsaturated fats — including polyunsaturated fats — both omega 3 and omega 6, as well as monounsaturated fats. You can look back to the preceding blog, if you aren’t clear on these.

Endogenous Fats

Our body actually makes fat in a process called lipogenesis. This is important because some of the LDL cholesterol and triglycerides (TG) that gets reported on blood test results is endogenous; that is, our bodies made it. So we have high LDL (“bad” cholesterol) or triglycerides it’s not all from the fat we eat!

[Not only do our bodies make saturated fat, but excess carbohydrates gets stored in our body first as triglyceride and then if it still isnt needed, it gets stored as LDL cholesterol in our liver.  So carbs can raise both triglycerides and LDL cholesterol.]

Below, I will present just enough chemistry to understand the different types of fat and more importantly, be able to read about them and understand.

The Saturated Fat Our Body Makes and What it is Used For

1. The first thing that you need to know is that palmitic acid is a long-chain saturated fat is made (synthesized) in the liver. Palmitic acid is a 16-carbon fatty acid and having so many carbons in its backbone, it is considered “long chain”). It has no double bonds, so all the carbons in the backbone have a hydrogen bound to it (more on that below), so palmitic acid is a saturated fat.  Palmitic acid is found naturally in foods such as butter, cheese, milk and meat — but it is also synthesized by our bodies!

Now the message of the media since the mid- to late-1970s is to eat low-fat dairy; including low fat milk, low-fat yogourt and low-fat cheese with the assumption that saturated fat is “bad” for us — but our bodies actually manufacture it!

2. The other thing that you need to know is that a triglyceride is made up of three fatty acids attached to a glycerol molecule. That’s easy to remember, because “tri” means “3”.

a) Glycerol acts as the support for the other fats and is made up of three carbon atoms, each with something called a “hydroxyl group” bound to it.

A hydroxyl group (written “-OH”) is an oxygen and a hydrogen molecule bound together.  That is, water (H2O) is just a hydrogen (H) molecule bound to a hydroxyl (-OH) group.

So, this is a glycerol molecule;

As you can see, each of the carbons in the chain have a hydroxyl (-OH) group bound to it. Easy, so far, right?

b) Fatty acids are long chains of carbon atoms (i.e. think of a freight train, where each rail car is a carbon atom) with a carboxylic acid (-COOH) group at one end (i.e. the caboose is a carboxylic group). At each of the carbons in the chain, there is the potential for a hydrogen atom (H) to bind there.

You may recall from our previous article that a saturated fat is one that has no double bonds in the carbon chain, so in that case, all the carbon atoms in the chain have a hydrogen attached.  It is having all the carbons “saturated” with hydrogen atoms, that make it a “saturated” fat!

The names given to fatty acids are based on the number of carbon atoms and the number of carbon-carbon double bonds in the chain.

Different Kinds of Oils 

Remember, a triglyceride is made up of three fatty acids attached to a glycerol molecule. So, for example, palmitic acid and stearic acid are both exactly the same, except one has 16 carbons (palmitic acid) and the other has 18 carbons (stearic acid) in its chain.

Palmitic acid, a saturated fat has 16 carbons.  That is, it is “saturated” with hydrogen atoms at each of its 16 carbons. It is all of this “saturation” that makes saturated fat solid at room temperature.

Stearic Acid, is also a saturated fat, but has 18 carbons, so each of its carbons has a hydrogen bound to it,

Using just these two saturated fatty acids (palmitic acid and stearic acid) we can combine them in different ratios to make entirely different oilsFor example, canola oil has a 4:2 ratio of palmitic acid to stearic acid and grapeseed oil has an 8:4 ratio of palmitic acid to stearic acid.

Furthermore, the same two fatty acids can be put together in the same ratio and be different fats. For example in a 7:2 ratio, it could be either almond oil or safflower oil — depending on how they are put together.

Palmitic acid, the saturated fat that our body makes is found in all kinds of “healthy” foods.

Lipogenesis – Our Bodies Making fat!

Lipogenesis is the process by which our bodies actually make fat and our bodies can make unsaturated fats or saturated fats.  

Unsaturated fatty acid lipogenesis

Our body can make a longer chain unsaturated fat from a shorter chain fatty acid (such as taking the linolenic acid from flax seed and adding carbons to the chain to make arachidonic acid). But there are limits.  Our bodies cannot take the linolenic acid from flax seed and make it into eicohexanoic acid or decahexanoic acid which are the healthy “omega 3 fats” fats found in  fish. So eating eggs made from chickens fed flax is not the same as eating fish.  We just can’t turn one into the other. Our body can make it longer, but not much longer.

Saturated fatty acid lipogenesis

As said above, our bodies synthesize palmitic acid, a 16 carbon saturated fat in our liver and then forms a triglyceride from three palmitic acid molecules attached to a glycerol molecule. These triglycerides are then transported around the body in something called a VLDL. More on that just below. 

Cholesterol – The Good the Bad and the Ugly

Most people know that HDL cholesterol is the so-called “good cholesterol” and LDL cholesterol is the “bad” cholesterol  — but where does LDL (“bad cholesterol”) come from? The first step when our body makes something called VLDL.

Very Low Density Lipoproteins (VLDL)

The body takes the triglycerides it manufactures in lipogenesis as well as takes in in the diet into Very-low-density lipoprotein (VLDL) cholesterol. These VLDLs move cholesterol, triglycerides and other lipids (fats) around the body.

VLDL is produced in the liver and include the triglycerides made with differing amounts of palmitic acid.  That is, our bodies MAKE palmitic acid in the liver and then combine the palmitic acid it makes in differing ratios, into triglycerides. It then takes the triglycerides, containing palmitic acid and protein and packages it into VLDLs. It then releases the VLDLs into the bloodstream, to supply body tissues with triglycerides.  About half of a VLDL cholesterol is made up of triglycerides, including those containing the palmitic acid it made!

High levels of VLDL cholesterol have been associated with the development of plaque deposits on artery walls, which narrow the passage and restrict blood flow.

VLDL cholesterol on blood test results aren’t measured, but estimated as a percentage of the triglyceride value.

What is LDL cholesterol?

When VLDL cholesterol reach fat cells (called “adipose tissue”), the triglyceride is stripped out and absorbed into fat cells. That means that VLDLs shrink.

Once a VLDL has lost a large amount of triglyceride it becomes a new, smaller, lipoprotein, which is called Low Density Lipoprotein, or LDL — the so-called ‘bad cholesterol’. LDL contains mostly cholesterol and some protein. Some LDLs are removed from the circulation by cells around the body that need the cholesterol contained in them and the rest is taken out of the circulation by the liver.

Here is the key point: the only source of LDL is VLDL. 

Saturated Fat — not dangerous and can be beneficial 

The media keeps telling us that “saturated fat is bad” and that it is even “dangerous” — but if it was so dangerous, why would our bodies actually manufacture it?  Our bodies manufacture palmitic acid, a saturated fat, then synthesize triglycerides from it which it sends all around our bodies, supplying our bodies with saturated fat!

Furthermore, there are some saturated fatty acids, called Medium Chain Triglycerides (MCTs) that are metabolized entirely differently than the longer chain saturated fatty acids and have beneficial properties.  These MCT oils go straight to the liver by the portal circulation and don’t need to be digested.

People who consume fats high in MCT oil, such as coconut oil which is almost half (44-55%) Lauric acid, an MCT have been found to have lower amounts of “belly fat” than those that do not consume these saturated fats.  Studies have found lower rates of “visceral adiposity” or “belly fat” in those that consume these fats, and correspondingly , lower lowering waist circumference.

Since carrying fat around the abdomen (the so-called “apple shaped” people) is considered to be a risk-factor to heart disease and studies have found that those who eat a diet high in MCT saturated fats have less fat around their middles and a smaller waist circumference, can we categorically say that saturated fat is really “bad” or “dangerous” to heart health. In fact, in our next article, we will outline the beginning of a change in the recommendations concerning saturated fat consumption.

Some thoughts…

Saturated fat and its consumption needs to be put into context; one context would be looking at the risks of a high carbohydrate diet compared with a high saturated fat diet, for example.  As covered in previous blogs, prior to 1977, when the dietary recommendations in Canada and the US changed to favour a diet low in saturated fat and high in carbohydrates, the rate of Diabetes was 1/10th what it is now and obesity rates in adults, especially men were too. Childhood obesity was almost unheard of prior to 1977.

Another context would be to differentiate between saturate fats.  That is, to look at which saturated fats.  Numerous studies demonstrate the benefits of MCT oils in increasing metabolism, lowering body fat, especially “visceral adiposity”.

Another context would be to determine how much of the “high cholesterol” (i.e. high LDL cholesterol) came from VLDL that was endogenously produced, versus eaten (exogenous).

Many studies have found that people are less hungry (have increased “satiety”) when they consume higher fat dairy products (which are rich in saturated fat), and as a result consume less calories overall than those that do not eat higher fat dairy products. So, we need to know which fats, and in particular which saturated fats are associated with this increased satiety?

It is my opinion that “vilifying” fat — labelling it as ‘unhealthy’ and the current government dietary recommendations and the media ads encouraging us to eat “low fat” everything, is creating a much bigger problem than the fat itself.  When manufacturers take out fat, they have to ‘replace” it with something and that ‘something’ is often sugar (simple carbohydrates).  Is increasing the carbohydrate content ‘safer’ than the naturally occurring fat that was found in the milk or yogourt or cheese, in the first place?

Recent studies seem to indicate that saturated fat consumption is not the issue when it comes to heart risk — and that saturated fat may actually be protective against heart risk. Certainly there are many studies showing the benefits of consuming MCT oil for reducing “belly fat”, which reduces heart risk — so can we say that something like coconut oil, used in moderation is “bad” or “dangerous”.

Looking at the epidemiological data from the last 35 years, we can see what has happened to obesity rates and diabetes rates since both the American and Canadian governments have been encouraging us to eat “low fat” everything.

Are naturally occurring fats really the issue — or are synthetic “trans fats” and excess carbohydrate?

At this point in time, I am persuaded by the many studies I have read, that naturally occurring fats, including saturated fat are not “bad” or “dangerous” when consumed as part of a whole-foods diet.

Note: Everyone's results following a LCHF lifestyle will differ as there is no one-size-fits-all approach and everybody's nutritional needs and health status is different. If you want to adopt this kind of lifestyle, please discuss it with your doctor, first.

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