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An Unfounded Fear of Fat

Many of you have previously attended our low-carb weight loss seminar and we’ve mostly cured you of your fear of fat. For the rest of you, that still need some reassurance that you DO NOT need to be counting fat grams or worrying about saturated versus unsaturated fats, here’s a quick breakdown of fats, in your diet and how they work in your body:

First of all, fat is essential. You must have it. Without it, your body will go into fatty acid deficiency and some of the symptoms or consequences of that are: scaly dermatitis, alopecia (hair loss), thrombocytopenia (too few or reduced platelets in the blood), and, in children, growth retardation. Think about this: your brain is over 60% fat. It takes only about 3% of dietary intake from fat to prevent fatty acid deficiency, as long as at least a small amount of that is coming from essential fatty acids (EFAs) such as omega-3-and-6.

Secondly, if you’re not eating enough fat, what are you eating in its place? Likely its carbohydrate, and as we’ve all learned before, too much carbohydrate intake, regardless of the sources leads to:

  • weight gain
  • hyperinsulinemia, which leads to: hypercholesterolemia, hypertension, inflammation, reduced kidney function or stress on the kidneys and insulin resistance
  • Chronic hunger

Types of Fat…How to Decipher the Terminology

So lately, the newest trend in the food and nutrition industry is labeling things with ‘good fat’ or ‘healthy fat’ etc. And then don’t forget ‘omega-3s’ and ‘omega-6s.’ The food industry counts on the fact that you, the consumer, knows relatively little about fats, what they do and what the terminology actually means. The latest tactic in the war on fat is to condemn saturated fat and applaud unsaturated fats. So lets take a look at different fats and then we’ll look at some of the research relating to those.

Fat 101:

First of all, a fat, or lipid, can take on many forms in nature or in the body. The main component of all fats, however is long carbon chains with hydrogens attached to each carbon like these examples below:

(you may need to click on the image to see it larger if it is hard to read in your browser)

Saturation: What does it mean?

A saturated fat is a fat that has no double bonds between carbon atoms on its chain. Saturated fats are usually always solid at room temperature and they are almost exclusively found in animal sources, however there are definitely a couple of plant sources that are highly saturated, such as coconuts. The more saturated a fat is, the thicker it will be in its natural form. Unsaturated fats are generally liquid at room temperature because they contain at least one, but sometimes many more, double bonds. This is when two carbons next to each other are bonded by not one, but two covalent bonds and each has one less hydrogen because of it. This is significant in nutrition because double bonds are highly reactive in your body. All it takes is a molecule with even a slight charge to break that double bond apart and let something bond to it, like free radicals and such. This causes a lot of damage to cell membranes if it happens in the wrong place, and in general, these unsaturated fats are usually quick to spoil and become rancid, unless those double bonds are created in processing as trans fats.

So now that we know what a fat looks like physically and chemically, lets look at what happens to it once you eat it.

Once the fat reaches your stomach, it triggers the release of gastric lipase, which does a small amount of fat digestion, however, the majority of fat digestion occurs in the small intestine. Once fat enters the duodenum (the upper or first part of the small intestine), bile is released from the gall bladder. Bile is a substance called an emulsifier. Essentially the bile salts bind to fat globules to keep them from clumping together in huge clumps of largely undigestible fat. When the bile salts keep the fat into smaller clumps, pancreatic liapses (enzymes from the pancreas that break down fat) can get to the fat molecules easier and break them apart, yielding short, medium and long chain fatty acids, mono-glycerides and di-glycerides. These fat molecules can now passively cross the cell membranes of your intestinal cells, where they are repackaged as triglycerides, some cholesterol and given protein carriers to form various  lipoproteins such as chylomicrons and mycelles. Then they are shuttled into your lymph system, which carries fat soluble nutrients that cannot go directly into your bloodstream because the high water content of your blood would cause the fat particles to precipitate out and clog things up.

The lymph system empties its contents into the thoracic duct, which eventually ends up carrying the fat molecules to your liver for processing. And here’s where people fall short on the ‘saturated-fat-is-bad-for-you’ hypothesis.

The liver packages cholesterol and fats into lipoproteins that circulate throughout your body in your bloodstream to bring these important molecules to cells that need them. Everyone has likely heard of ‘good cholesterol (high density lipoprotein or HDL)’ and ‘bad’ cholesterol (low density lipoprotein or LDL). Those are two types of cholesterol that circulates as a lipoprotein but you also have VLDL (very low density lipoprotein) that is of the light and fluffy kind, full of big fat molecules that get picked off rather quickly, not causing problems. High density lipoprotein carries cholesterol and fats to the liver for recycling once cells have used what they want. LDL cholesterol carries cholesterol and fats to the cells for use. VLDL also carries cholesterol and fats to the cells for use.

What is wrong with thinking in terms of good and bad cholesterol? Well, the current hypothesis (and yes its a hypothesis because it has not been proven, rather, it has been disproven by a few studies, but we won’t mince words here) is that high levels of LDL cholesterol put you at higher risk for heart attacks because the LDL cholesterol will bind to artery walls and form hardened plaques. Those plaques  harden the arteries, making them less elastic, thereby causing the heart to work even harder to pump blood through them (remember the post about blood pressure?). This eventually leads to heart failure. However, another supposed consequence of LDL is that it will build up in cardiac arteries (the main arteries carrying blood and nutrients to the heart’s muscles) which leads to a myocardial infarction, or heart attack, because the muscles cannot get enough oxygen to pump and they stop pumping, stopping the heart. Here’s the problem with this hypothesis:

  • Here is a research article published in the Journal of the American Medical Association. In this project, researchers looked at the trends of LDL cholesterol levels in Americans and compared it to rates of heart attacks, because they were out to prove that higher LDL cholesterol levels mean you will have more attacks. However, they found from the data that as LDL cholesterol levels declined and were the lowest, heart attack rates did not statistically change. That’s right. With lower LDL cholesterol levels, heart attacks were just as common as with higher LDL cholesterol levels. Then the researchers, in finding that their hypothesis was not supported, switched and baited and pointed out that many more people could be taking statins to lower their cholesterol than are taking it. Wow. So your hypothesis wasn’t supported, but you still feel like people should take a drug for a condition that it may or may not even help.
  • The famous Framingham study, which set out to monitor diet and compare it to factors that were believed to contribute to heart disease, fell short of proving that dietary saturated fat and cholesterol had any effect at all on serum cholesterol (cholesterol circulating in your blood). The researchers buried the results that actually proved that there was no connection between these factors (you can read more about this here on the blog of Dr. Eades). However, to this day, this study is heralded as ground-breaking, as long as you don’t actually dig up and look at the data the original researchers suppressed that made them look ridiculous. Here is but one excerpt from the data that were suppressed and later released: “There is no indication of a relationship between dietary cholesterol and serum cholesterol level. If the intake on animal fat is held constant there is still no relation of cholesterol intake to serum cholesterol level. If (further) a multiple regression is calculated [using animal fat and dietary cholesterol] there is also little suggestion of an association between this pair of variables and serum cholesterol level.”
  • In the Seven Countries Study, which was supposed to have shown that dietary saturated fat intake increased risk for heart disease and raised cholesterol levels, actually showed that in the countries compared, men with similar levels of serum cholesterol (anywhere from 180-250 mg/dL) had grossly varying rates of heart attacks. There was no standard showing that a high cholesterol level (generally considered anything over 100 mg/dL) made the participants any more at risk for heart attacks than did a lower cholesterol level. And the rates were across the board, regardless of the region of the world or the ethnic background of the participants. You can read more about that here.
  • And last but not least I’ll leave you with this article. It describes, in a very well written way, the path a couple of researchers took to arrive at the conclusion that the SIZE of the LDL particles is really what matters. If LDL particles are small and dense, then yes, they are much more likely to lead to heart disease or heart attacks. If LDL particles are big and fluffy, there is virtually no risk. However, the catch here is that when a lipid panel is ordered by your physician, they do not report the particle sizes, nor do they routinely screen for those at most medical institutions. We certainly have the capability to do so, but its not yet common practice, as many old school medical professionals don’t want to admit that maybe they’re not totally correct in stating that LDL cholesterol is bad.

I’ll leave you there with that much to digest and we’ll pick back up next time with a, hopefully, much shorter post examining why certain types of dietary fats are better than others, and its not what you’re being told by the American Heart Association, either.


8 responses »

  1. combatcrossfit

    Wow, I guess when I don’t post, nobody posts…
    I haven’t been writing down what I’ve been eating so I will start with today because its the only one I can thoroughly remember
    Breakfast: 2 soyjoy bars, almond milk
    snack: trail mix
    lunch: burrito bowl with veggies, ground beef, sour cream, cheese and salsa and lettuce
    snack: sweet potato fries
    dinner: chipotle bowl with veggies, barbacoa, salsa, guac, cheese
    snack: almond butter

  2. I have sucked on posting this week so I will do a condensed version:
    Sunday- breakfast; fasted due to a cheat meal the night before, lunch; chicken with plantains, Dinner; chicken, shrimp, and broccoli
    Monday- breakfast; protien shake, lunch; chicken breast with honey, Dinner; shrimp with veggies
    Tuesday- breakfast; protien shake, lunch; chicken breast and grapes, dinner; chicken and platains
    Wednesday- breakfast; omelet(turkey bacon, mushrooms, little bit of cheese), juice from our juicer, late lunch; shrimp soup, dinner: ice cream
    Thursday- breakfast; protien shake, lunch; leftover shrimp soup, dinner; chicken with honey and plantains.

  3. I have sucked at posting also so I am just going to start from yesterday and do my best to keep up from here on out.

    Breakfast – trail mix ( i had an early meeting and didn’t have time to prepare anything. This mix has zero salt, walnuts, almonds, raisins, sunflower seeds and pumpkin seeds. Its seem to help with the hunger)
    Lunch – huge piece of grilled Cod with half a sweet potato
    Snack – trail mix
    Dinner – huge protein shake after WOD
    Snack – trail mix with some chocolate hazelnut butter small glass of milk

  4. combatcrossfit

    This has nothing to do with what I’ve eaten today, but Wayne told me this morning that there were some huge plumbing trucks at the new space getting ready to work on that plumbing!!! excited…..

  5. sweet!!!

    Cant wait to get into the new, bigger space!!!!!!

  6. Me three I have sucked at posting this week! Here we go
    Breakfast-protein shake
    Lunch-chicken breast w/apple
    Dinner-chicken breast w/broccoli
    I have to think about the rest of the week I will get back to you guys.

  7. Sunday Nov. 7
    Breakfast- 5 eggs 3 with yokes and 2 whites and a banana.
    Lunch- chili
    Snack: sweet potato chips
    Dinner: chili w/ 2 meatballs
    Bedtime: protein shake

  8. Monday Nov. 8
    Breakfast: Omelet w/green peppers and bacon.
    Lunch: chili w/apple
    Dinner: chili w/plantains


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