Saturated Fats: Friend, Foe, or Don’t Know?

It usually goes like this…

“But fat and cholesterol increase cholesterol”, my client said.

“So which cholesterol does it increase?” I responded.

“The doctor said the ‘bad one’”.

Without question, this is the most common discussion I get into with anyone who has an inkling of interest in nutrition and taking care of their health. Trying to reverse deeply ingrained beliefs that have the support of governmental agencies and public outlets is a tough nut to crack.

In this article, I want to go briefly into why you should not believe every negative stereotype you have heard about fat, particularly saturated fat, and cholesterol. Now before we move on, let me make it clear that I am not stating fats and cholesterol are not dangerous; they absolutely can be given the right (or wrong) situation—namely genetics, existing physiological stress, and general lifestyle.

A prime example of how saturated fats and fats in general can negatively affect health is a rare genetic disorder people are born with called familial hypercholestermia. In this condition, people lack a gene that allows the body to get rid of LDLc from the bloodstream. Typically, these people will show normal HDL and triglyceride (TG) levels, but their LDLc levels will be through the roof, ranging from 350-1000 mg/dL (a healthy person might exhibit 100 mg/dL). Sometimes, you can’t win against genetics

Also not surprisingly, a high-stress lifestyle puts you at an increased risk of heart disease. The reason is not because you are probably eating a bit too much fat, but because chronic stress puts your body in a state of inflammation, which in turn damages your arteries, increases your blood pressure, and forces your body to go haywire.

My point is that any food can be turned from an angel to a devil. Dietary fats, and cholesterol, have a relative health effect (RHE) on you, just like protein and carbohydrates do. But if you keep a good bill of health, the net effect is a positive one.

What is fat?

Fats, or lipids, belong to one of the three main MACROnutrients, nutrients that supply you with energy, are measured in larger quantities than vitamins and minerals, and play extremely important structural and metabolic roles in the body. Though they top the energy-supply chart by giving you 9 calories per gram, their main job is not to make you fat, but to supply you with long-term energy so you can function and continue plugging away at Facebook.

Since this is not a biochemistry crash course, I will make it as simple as possible so both you and I can understand. Last thing I want to do is confuse myself. Dietary fats are categorized into four groups that have distinct molecular properties and functions. Over the course of a couple of posts, I will go over each fat, but today, we will cover saturated fats.

  1. Saturated fat (SFA)
    1. No double carbon bonds
    2. Solid at below room temperature; spreadable at room; and liquid at above
    3. Stable under high heat (cooking, baking), so makes for suitable cooking oil
    4. Several types of SFA, each with its own effects on health
    5. Since no double bonds, generally does not go rancid and as such, more stable inside the body as well
    6. SFA are required to make sex hormones (testosterone, estrogen); they make up over 70% of the cells in the body; burn in a safer and more efficient manner than glucose
  2. Mono-unsaturated fat (MUFA)
    1. One double carbon bond
    2. Liquid
    3. More stable under high heat, though this depends on the type of plant the oil is from
    4. Since only one double bond, less prone to rancidity, but high heat can damage it
    5. Most make for suitable cooking oil (olive oil excluded)
  3. Poly-unsaturated fat (PUFA)
    1. Two or more double bonds
    2. Liquid
    3. Unstable under high heat, though this depends on how much processing it went through during production
    4. Since it has several double bonds, very prone to rancidity and can cause oxidative damage
    5. Not a suitable cooking oil
    6. PUFA are a function part of the cell membrane, giving cells its fluidity
  4. Trans-fatty acids (TFA)
    1. Originally a saturated fat, but partial hydrogenation modifies the melting point and allows TFA to be solid at room temperature
    2. Products with TFA in them have longer shelf-life
    3. Stable under high heat and long storage
    4. TFA can be found naturally in foods (dairy, meats) and manufactured on a larger scale by food producers (most common source of TFA in current American diets)

Goodie, you know the four main fats. Now what? What about Saturated Fats’ effects on your health?

Based on the properties of the fats above, if you read between the lines and thought, “saturated fats” don’t seem to be so bad then my job with this article would be done. However, I am sure we all need some clarification.

Over the past fifty years, SFA has gotten a lot of bad press, mainly for its ability to increase cholesterol levels and thereby its theorized ability to increase heart disease risk. Back then, research was not as meticulous, but now we have more and better insight. Studies have been carried out in rodents and humans in randomized trials and researchers kept track of hundreds of thousands of people in cohort studies. In short, there is no good reason to believe that saturated fat is the culprit in heart disease. In fact, much of the hype in the past was not based on studies done on humans, but by speculation and… injecting rabbits with liquid cholesterol. Why do I bring this up? Because a rabbit’s natural diet does not contain cholesterol. They eat plants.

But cholesterol isn’t part of my natural diet!

For one, it’s nearly impossible to isolate one nutrient and study its overall effect on health. Even if all you ate was butter, you wouldn’t be able to measure it. Why? Because eating only butter creates a nutrient imbalance detrimental to health that is independent of saturated fat. To function at peak health, your body also needs protein and carbohydrates.

No matter how many times I state, “saturated fats do not independently increase your risk of heart disease,” it just seems to leave a blank stare on people’s faces. I don’t blame you for reacting the same way. For years, we have been told that saturated fats are bad for health. Most times, if you went to a doctor’s office with high cholesterol, the doctor won’t even ask you about your diet. They may ask you about exercise and what you do.

Doc: “Do you exercise?”

You: “Yes.”

Doc: “Ok.”

Ok, perhaps I should give this doctor a bit more credit.

Doc: “How much?”

You: “I go to the gym 3 times a week.”

Doc: “Ok.”

Next, they will take a quick look at your numbers, probably the LDL cholesterol (LDLc), and if they are not pointed in the right direction, will suggest you either “fix your diet” or try to hand you a prescription for a drug that has side effects. Great!

So what do your lab results mean?

According to the National Cholesterol Education Panel (NCEP), here are ‘normal’ guidelines for lipids:

LDLc: <100 mg/dL
HDLc: > 60 mg/dL
Total Cholesterol: <200 mg/dL
Triglycerides (TG): <150 mg/dL

The LDLc numbers only tell some of the story. Over a decade ago, researchers found out that there are actually two types of LDLc particles—small and large. Small LDLc particles have been shown to be atherogenic—promote heart disease—because they are more likely to get stuck in holes in the arterial wall, whereas large LDLc particles are benign and less likely to get stuck (6). Now the thing to note here is that even if two people had the same concentration of LDLc in their blood, their atherogenic profile will differ. In other words, if one person had an LDLc of 100 mg/dL but it represented large particles, they would be at a reduced risk of heart disease.

Saturated fats have been unjustly vilified and LDLc alone is a poor predictor of heart disease

While I say that saturated fats have been unjustly vilified, that is not permission to go whole-hog on saturated fats. It’s true that research has focused on how saturated fats influence health and found that saturated fats are not the criminals they were thought to be, but it’s also important that you have a balanced intake of fat. According to research and observations, it’s prudent to have most of your fats come from a combination of SFA and MUFA, as this combination has been shown to improve the LDL/HDL ratio, especially in women (9).

But if you turn your attention back to how SFAs negatively affect health, you will see that this theory just does not pan out. In 2010, a meta-review was released in the American Journal of Clinical Nutrition, what dietitians consider to be the holy grail of nutrition research. Here, the study went over 21 prospective epidemiological studies that tracked over 347,000 people. What’s ironic is that one of the researchers of this study, Ronald Krauss, used to be in the anti-fat camp, until he actually looked at the literature and came to his own conclusions. They concluded:

“There is no significant evidence concluding that dietary saturated fat is associated with an increased risk of CHD (coronary heart disease) or CVD (cardiovascular disease)” (1)

Research has also repeatedly shown that SFAs in and of themselves are not harmful to your health. To elucidate this a bit, researchers used 48,000 postmenopausal women from the Women’s Health Initiative program, one of the largest and longest running studies that observed how nutrition, exercise, and lifestyle influenced health, and put them into a modification trial where they can measure how specific parameters influence study primary outcomes. In this case, if decreasing saturated fat over time would decrease CVD risk. Over an average of 8.1 years, total fat intake decreased by 8% and saturated fat by 3%, while consumption of fruits, vegetables, and grains increased. Here is what they had to conclude:

“Over a mean of 8.1 years, a dietary intervention that reduced total fat intake and increased intakes of vegetables, fruits, and grains did not significantly reduce the risk of CHD, stroke, or CVD in postmenopausal women and achieved only modest effects on CVD risk factors” (3).

Ok, “but what about the more specific stuff that saturated fat does, like how experts say that since SFAs increase cholesterol, they also increase your risk of heart disease”?

The above general statement is almost false. SFAs have different chain lengths, and each impart a different effect on health, so to say a blanket statement like above does not take into account the various properties of SFAs. In fact, most of the SFAs have a neutral effect on health, with a few having a positive effect while one having a negative one. SFAs, while they do increase LDL cholesterol, also increase HDL cholesterol, thereby not changing the ratio of total cholesterol to HDL cholesterol, a strong predictor of heart disease risk (2). Additionally, SFA are the strongest at lowering TG levels. From the abstract:

“Lauric acid greatly increased total cholesterol, but much of its effect was on HDL cholesterol. Consequently, oils rich in lauric acid decreased the ratio of total to HDL cholesterol. Myristic and palmitic acids had little effect on the ratio, and stearic acid reduced the ratio slightly. Replacing fats with carbohydrates increased fasting triacylglycerol concentrations.”

Above I mentioned that replacing SFA with MUFA improved LDL/HDL ratios, but it seems that improving, or lowering, your Total Cholesterol/HDL ratio is even better. Also, that last bit is interesting, right? Basically it’s saying that eating carbohydrates instead of fats will increase fasting levels of triglycerides, an independent risk factor for heart disease in both men and women. Another time, another place.

The feverish chase of linking SFA with heart disease has slowed down quite a bit, and I think it’s probably because people have finally come to the realization that not only is it unfair to ostracize SFA, but also because SFAs don’t independently increase the risk of heart disease.  As of this writing, not much more literature on saturated fat and health has been published. Nonetheless, studies continue. One of the few more recent ones I could find was this bit, again from the Journal of Clinical Nutrition. They concluded:

“The effect of diet on a single biomarker is insufficient evidence to assess CHD risk. The combination of multiple biomarkers and the use of clinical endpoints could help substantiate the effects on CHD. Furthermore, the effect of particular foods on CHD cannot be predicted solely by their content of total SFAs because individual SFAs may have different cardiovascular effects and major SFA food sources contain other constituents that could influence CHD risk” (4).

This is Harvard’s way of saying, “we should not implicate only saturated fats as a cause for heart disease, but a variety of factors, including smoking, exercise, genetics, and general dietary habits”. The second one was from the Journal of Clinical Lipidology. Their conclusion was much in line with the above, but there was even more skepticism about the negative health effects of SFA and the beneficial health effects of even MUFA and PUFA.

“High-density lipoprotein (HDL)-C increases with SFA intake… among individuals who are insulin resistant, a low-fat, high-carbohydrate diet typically has an adverse effect on lipid profiles (in addition to decreasing HDL-C, it also increases triglyceride and LDL particle concentrations). Consequently, a moderate fat diet in which unsaturated fatty acids replace SFAs and carbohydrates are not augmented is advised to lower LDL-C”. (5).

The above conclusion should be a bit of a head-scratcher. Why would they advise that people replace SFA with MUFA to decrease LDL when, just a couple lines before, they clearly stated that SFA increases HDL? Based on this, it is prudent to have a good combination of SFA and MUFA, but not to be scared of SFA in the absence of a high carbohydrate diet. More importantly, two of the authors of the above study, Drs. Walter Willet and Alice Lichtenstein, were initially anti-fat and believed SFA to be a culprit in heart disease. Again, I think it is extremely liberating that researchers who once advised against SFA intake are beginning to question their original theories and even do an about-face.

And a review done in 2013 showed that full-fat dairy products had this to conclude:

The observational evidence does not support the hypothesis that dairy fat or high-fat dairy foods contribute to obesity or cardiometabolic risk, and suggests that high-fat dairy consumption within typical dietary patterns is inversely associated with obesity risk” (10).”

Of course, we can’t just accept wholeheartedly that SFA cause no damage. As I mentioned before, they can. But the science is stacking up in favor of exonerating SFA. There is no cold-hard truth, but there hardly ever is in science. If there was, scientists would be out of a job and there would be no more need for ongoing research.

“By the way, I like cheese, yogurt, and butter. What about them?”

Dairy products make up a group of foods that have the highest concentration of saturated fats, collectively. One serving of Camembert cheese has 7g of fat, 4 of it being saturated. One 7 ounce serving of full-fat Greek yogurt has 10-12g of fat, 8 of it being saturated. And one tablespoon of butter has 12g of fat, 8 of it being saturated. They also taste a whole lot better than their chalky non-fat counterparts.

So where am I going with this? In addition to the last study I quoted above, there’s more good news for those of you who like full-fat dairy goodness: a most recent study published online in August 2014 showed that two full servings of full-fat Camembert cheese or yogurt per day over the course of 8 weeks had no negative impact on people with elevated cholesterol and taking no medications (7). This study is followed nicely in the footsteps of a study done earlier in 2014 showing that full-fat dairy reduced the risk or prevented cardiometabolic disorders, even in randomized trials (11).

But this is not news. Studies dating back to the early 2000’s show full-fat dairy products improve health and weight-loss. Whereas cheese improves LDLc more than butter, butter improves HDLc more than any other dairy product (8).

What about eggs?

Ah, the venerable, honorable, and revered egg. There’s nothing quite like it. Indeed, nothing quite like eating nature’s perfect food that comes out of an… anus? Ok, technically, it’s not the anus but a ‘cloaca’. But enough of the technicalities.

Eggs are always a hot topic. Though they are not as high in concentration of saturated fats, they do concern most people when it comes to cholesterol levels. Egg yolks contain nearly all of the nutrition of the egg. It is one of the few natural sources of choline, contains magnesium, vitamin A, and a range of B-vitamins. In essence, whole eggs are one of nature’s perfect food.

In research, there is an ongoing tug-o-war when it comes to egg consumption. On one hand, eggs have been shown to increase HDL levels and converting LDLc into the large particle sizes (12). The mentioned study, done in 2006, showed that eating four eggs per day benefited health in the general population. More studies done later, like these 2010 and 2013 ones, showed that eating three eggs per day improved LDLc and HDL profiles while simultaneously increasing blood antioxidant status, especially during a lower carbohydrate diet (13, 14).

On the other hand, research has shown that eating more than one egg per day has no impact on cardiovascular risk, but may pose a risk to those with type 2 diabetes. At the same time as increasing the risk of heart disease to those with type 2, egg consumption decreases the risk of stroke. Some of these studies were done using egg questionnaires that ask participants to estimate how many eggs they eat per day, over the course of years (15). Can you remember how many eggs you ate last year? Interestingly enough, the study done in 2013 showing beneficial effects touched on how egg consumption can benefit type 2 diabetes.

“Daily intake of 3 whole eggs, as part of a CRD [carbohydrate restricted diet], increased both plasma and lipoprotein lutein and zeaxanthin [antioxidants]. Egg yolk may represent an important food source to improve plasma carotenoid status in a population at high risk for cardiovascular disease and type 2 diabetes (14)”.

 As you can see, the research is not as clear-cut on egg consumption. But by combining both observation and research, I have come to conclusion. Whole egg consumption does not increase your risk for heart disease. In fact, previous clients not only noticed beneficial effects on cholesterol, but also on weight status, blood pressure, and blood sugar control.

Wrap up and we’re not talking about a Big Mac to go

The best way to improve your cardiovascular disease risk and general health seen through lipid test results is to not only decrease and optimize your LDLc, but also to decrease TG. When you turn both of these numbers for the better, your HDLc will naturally go up. How do you achieve these feats? Eat less refined carbohydrates and more SFA and MUFA.

Again, this article’s purpose is not to get you to eat more saturated fat, although it’s definitely not deterring you so. If your preference is to stay away from saturated fat, that’s your decision. The goal of this article is to enlighten you, stating that there’s no reason to be scared of saturated fat in the presence of a whole foods diet. If you’re eating a Standard American Diet that consists of Oscar-Meyer bacon, cheese so processed it can only be called ‘cheez’, and freezer-burned French fries, then adding saturated fat will do more harm than good. But let’s make it known that it’s not the saturated fat that’s doing the damage, it’s the diet.

Can you see yourself having good health after eating like this?

Perhaps you want to start replacing your rancid and unhealthy polyunsaturated fats—cottonseed, peanut, canola, corn, soybean, safflower, and sunflower—with saturated fats and reap the benefits. Here are some sources. Take note how these sources are also whole foods that taste good, unlike the PUFAs that we are all commonly told to consume.

  • Egg yolks
  • Fattier cuts of animal meat
  • Greek yogurt, kefir, cottage cheese, milk (not a huge fan of milk for reasons outside the scope of this article), cheese
  • Coconut products (especially extra virgin coconut oil)
  • Grass-fed, organic cow, goat, sheep butter
  • Beef tallow and pork lard (though the fatty acid composition of these two are highly dependent on how the animals were raised)

And in case you are wondering…

I will include my n=1. I try to refrain from doing this too much because I apparently lack age. And many people will be quick to point out that, “I am young and active” and that I “will soon see the negative effects of eating the way I do”.

Except, I won’t. Stop to take a look at all of the sick and obese teenagers. More than 60% of these kids will develop type 2 diabetes later in life and will probably die of heart disease; but not before going blind or losing their hands and feet. I am 28, so unless I come down with an unavoidable genetic disorder, chances are extremely low that I will succumb to heart disease based on the research and my lab results.

I have a family history of high cholesterol, high blood pressure, peptic ulcers, and stroke. Both of my grandfathers died in their early 60’s of a stroke, my aunt had half of her stomach resected, and my mother is currently on blood pressure, cholesterol, ulcer, and arthritis meds. The most ironic thing about my mother’s diet is that she eats hardly any saturated fats yet has high cholesterol. She doesn’t drink, smoke, doesn’t even work part-time, but she is currently eating the very same “heart healthy” vegetable oils peddled by our government agencies. If only she would listen to what I say to her.

My diet mainly consists of whole fat Greek yogurt, kefir, grass-fed butter, coconut oil, chicken thighs, salmon, beef stew, whole eggs, loads of vegetables, and berries. I eat most of my calories at night, especially my carbohydrates, I fast 12-hours a day, and I exercise three times a week. Much less than your normal gym-rat who believes fat and cholesterol are bad for you. So my last blood work showed some peculiar yet predictable results.

Total cholesterol: 179
LDL: 101
HDL: 67
TG: 60
Fasting blood sugar: 90 mg/dL

Not too bad coming from a person born into a sick family.

Your main takeaway from this article is this:

Unless you have a genetic disorder or just flat out don’t like saturated fats, there’s no need to fear saturated fats. Like proteins and carbohydrates, they have an RHE, which can either be made better or worse depending on your circumstances. In the presence of a high carbohydrate diet, especially one composed of refined carbohydrates, SFA can do damage. But in the absence of a high carbohydrate diet, SFA not only improve HDL, triglyceride, and blood sugar levels, but they also provide you with a clean burning energy source.

As always, I appreciate your feedback.

Live life strong,




  1. Siri-Tarino PW1,Sun Q,Hu FBKrauss RM. Meta-analysis of prospective cohort studies evaluating the association of saturated fat with cardiovascular disease. Am J Clin Nutr. 2010 Mar;91(3):535-46.
  2. Mensink RP1,Zock PL,Kester ADKatan MB. Effects of dietary fatty acids and carbohydrates on the ratio of serum total to HDL cholesterol and on serum lipidsand apolipoproteins: a meta-analysis of 60 controlled trials. Am J Clin Nutr. 2003 May;77(5):1146-55.
  3. Howard BV1,Van Horn L,Hsia J, et al. Low-fat dietary pattern and risk of cardiovascular disease: the Women’s Health Initiative Randomized Controlled Dietary Modification Trial. JAMA. 2006 Feb 8;295(6):655-66.
  4. Astrup A1,Dyerberg J,Elwood P, et al. The role of reducing intakes of saturated fat in the prevention of cardiovascular disease: where does the evidence stand in 2010? Am J Clin Nutr. 2011 Apr;93(4):684-8.
  5. Baum SJ1,Kris-Etherton PM,Willett WC, et al. Fatty acids in cardiovascular health and disease: a comprehensive update. J Clin Lipidol. 2012 May-Jun;6(3):216-34.
  6. Cromwell WC1,Otvos JD. Low-density lipoproteinparticle number and risk for cardiovascular disease. Curr Atheroscler Rep. 2004 Sep;6(5):381-7.
  7. Schlienger JL1,Paillard F,Lecerf JM. Effect on blood lipids of two daily servings of Camembert cheese. An intervention trial in mildly hypercholesterolemic subjects. Int J Food Sci Nutr. 2014 Aug 6:1-6
  8. Nestel PJ1,Chronopulos A,Cehun M. Dairy fat in cheese raises LDL cholesterol less than that in butter in mildly hypercholesterolaemic subjects. Eur J Clin Nutr. 2005 Sep;59(9):1059-63.
  9. Müller H1,Lindman AS,Brantsaeter ALPedersen JI. The serum LDL/HDL cholesterol ratio is influenced more favorably by exchanging saturated with unsaturated fat than by reducing saturated fat in the diet of women. J Nutr. 2003 Jan;133(1):78-83.
  10. Kratz M1,Baars T,Guyenet S. The relationship between high-fat dairy consumption and obesity, cardiovascular, and metabolic disease. Eur J Nutr. 2013 Feb;52(1):1-24.
  11. Astrup A. Yogurt anddairyproduct consumption to prevent cardiometabolic diseases: epidemiologic and experimental studies. Am J Clin Nutr. 2014 May;99(5 Suppl):1235S-42S.
  12. Fernandez ML. Dietary cholesterol provided byeggsand plasma lipoproteins in healthy populations. Curr Opin Clin Nutr Metab Care. 2006 Jan;9(1):8-12.
  13. Mutungi G1,et al. Eggsdistinctly modulate plasma carotenoid and lipoprotein subclasses in adult men following a carbohydrate-restricted diet. J Nutr Biochem. 2010 Apr;21(4):261-7.
  14. Blesso CN1,Andersen CJ,Bolling BWFernandez ML. Egg intake improves carotenoid status by increasing plasma HDL cholesterol in adults with metabolic syndrome. Food Funct. 2013 Feb;4(2):213-21.
  15. Rong Y1,Chen L,Zhu T, et al. Egg consumption and risk of coronary heart disease and stroke: dose-response meta-analysis of prospective cohort studies. BMJ. 2013 Jan 7;346:e8539.

Eating Made Simple and Flexible

I got a question from a client the other day: how would I classify my dieting?

First off, I don’t truly believe in the words ‘diet’ or ‘dieting’ in the way that they are used and perceived these days.  I believe in an eating lifestyle, an approach that requires you to make behavioral and lifestyle changes to see results for a very long time. Sometimes this lifestyle calls for a ‘plan’ that you use to achieve a certain goal. Sometimes, you have no plan at all and just eat whatever the hell you want. Using this same logic, a ‘diet’ could cause someone to not only lose weight, but also to gain weight. But in our society, people are so wrapped up in the idea that a diet is used to lose weight that they lose sight of the multitude of other effects diets have on health. Hence, I prefer not to use a term that has a social stigma attached to it.

Asides from what I call my ‘dieting’ philosophy, I generally use the ‘If It Fits Your Macros’, or IIFYM, principles. In fact, this isn’t my dieting philosophy at all. I didn’t create it, nor did I help to. I chose to go this route because I feel it provides the most ‘flexibility’ when it comes to food choices. Extremely reputable people like Alan Aragon, Layne Norton, and Eric Helms spear-heading it helps, too.

So, what is IIFYM?

Essentially, you establish, track and try to eat your marconutrient, or macro, goals. Your macronutrients are the food nutrients that are measured in grams and used for energy–fats, protein, carbohydrates. Like any other eating plan, it does require making sure you are eating within the parameters of your goals, but it allows ‘flexibility’ in that it does not condone you for eating junk, so long as you don’t exceed your fat, protein, or carbohydrate daily targets. In so many words, you can substitute macronutrients for macronutrients.



This type of eating plan does not dictate that you stay ‘clean’ (whatever the hell that means) 6 days out of the week and then cheat at the end (although this is a plan that works well for many people). If you have intense chocolate cravings at 3PM, why wait? Just eat it and adjust your following meals accordingly (of course this isn’t optimal).

‘But if I don’t eat clean, what do I eat?’ See the picture above. You don’t need to live on chicken cutlets, steamed broccoli, and brown rice.

Anything you can eat and break down for energy–doughnuts included–contains fats, protein, and/or carbohydrates. A doughnut will have carbohydrates (sugar), fat, and some protein. Therefore, if you want a doughnut, you will eat a doughnut, but ensure that it replaces, not adds, to what you would normally eat. If a doughnut has 50g of carbohydrates and you planned on eating a 1/2 cup of rice, then you would eat a doughnut and not rice. Simple, right?

Why do I feel this is effective? Because for long-term results, moderation and motivation are key. I am willing to stake my life on the theory that more people will adhere to eating plans better if they are allowed a little bit of junk on a consistent basis rather than a lot of junk on a seldom basis. Why do I think this? Because my clients tell me so. As a trainer, I work with people of varying backgrounds. They are businessmen, or women, photographers, bankers, or housewives. Many of them simply cannot stay ‘clean’ until the weekend because of business functions. But as long as they know how to read food labels (and you should, more on that later), they are in safe waters.

At first, understanding and undertaking IIFYM may seem intimidating. What foods contain what? How do I calculate the rest of my macros if I eat this raspberry truffle? Is it OK if I add 1/2 teaspoon extra of olive oil? By the way, 1/2 teaspoon of olive oil won’t make a lick of difference. But keep practicing and it becomes mechanical, like driving, and you will only reap the benefits: freedom.


With that out of the way, let’s get into how to break down IIFYM into what you readers really want to see: numbers and guidelines. Before we move on, you should know that the protein and fat numbers are based on target bodyweight, or what you want to weight in 3-6 months.

Protein: I generally like to start clients at 1.0g per pound of target bodyweight, unless they are severely overweight.

Fats: I generally set this at 0.4-0.5g per pound of target bodyweight.

Carbohydrates: This depends on a client’s goal. However, I generally do not dip below a client’s amount of lean body mass (LBM), or total body weight minus fat mass. For example, if you are 180 pounds and know that you have 20% bodyfat, then you make this calculation: 180 * .20 = 36 —> 180 – 36 = 144 pounds of lean body mass. On any given eating plan, you will not go below 144g of carbohydrates per day. What if you don’t know your LBM? Then I suggest starting your carbohydrates at 150g.

For fat-loss: I generally prescribe clients to eat enough carbohydrates to cover their LBM in grams or 1.25 of it per day.

For muscle-gain: I generally prescribe clients to eat enough carbohydrates to cover 2.0 times their LBM per day.

Let’s use the above hypothetical trainee who weighs 180 pounds, carries 20% body fat, and wants to lose 10 pounds.
Protein: 170g per day, spread out evenly over meals
Fat: 85g per day
Carbohydrates: at least 144-180g per day

Like with any other eating plan, monitor your progress. After two weeks, if you do not see the scale move, then nudge calories in the appropriate direction.

Wrapping up, I feel that IIFYM is an optimal way to structure your eating plan. It provides you the reprieve of going ‘out of bounds’ without feeling guilty, but also allows you maintain a sustainable lifestyle. After all, research shows that over 90% of dieters cannot maintain their efforts after two years. What good is dieting if everything you have done falls apart after two years? Worse yet, those dieters who revert back re-gained all of their weight and then some.

If you have any questions, don’t hesitate to ask.