One of the most important analysis of dietary guidelines of the past decades came out last year in Nutritional Journal covering a wide range of topics including saturated fats. This analysis specifically looked at the dietary recommendations for Americans even as the obesity, diabetes, cardiovascular disease, etc. rates continue to rise massively in the US and in most industrialized countries.
Let's go back to the beginning.
There are two main hypotheses to describe the development of cardiovascular disease (among other factors). These are the lipid hypothesis and the chronic endothelial injury hypothesis. Currently, the lipid hypothesis predominates the medical industry; however, as stated in the above analysis of the data there is evidence that may show that it is based, at least partially, on incorrect science.
http://en.wikipedia.org/wiki/Lipid_hypothesishttp://en.wikipedia.org/wiki/Chronic_endothelial_injury_hypothesisOne recent movie, Fat head, looked at exploring the origins of why the lipid hypothesis is supposedly based on faulty science. A bit more on that here:
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Having looked into the science, I personally do not support the lipid hypothesis and I will detail information later regarding saturated fatty acids and cholesterol later with studies to support why it is likely incorrect.
Let's take a step back.
So what do saturated fats do in the body? What does cholesterol do in the body?
Saturated Fat
There are multiple sources of dietary fatty acids. Lauric acid (12), Myristic acid (14), Palmitic acid (16), and Stearic acid (18) are some of the most common. The only difference between these fatty acids are how many carbons are in the chain length, but as we shall see each of these have different effects on the body.
http://en.wikipedia.org/wiki/Lauric_acidhttp://en.wikipedia.org/wiki/Myristic_acidhttp://en.wikipedia.org/wiki/Palmitic_acidhttp://en.wikipedia.org/wiki/Stearic_acidShort chain triglycerides I'm going to briefly mention since we have little control over intake of them (as our gut bacteria produces them). However, if you have had issues with digestive problems, food poisoning, and anti-biotics where your gut flora has been decimated it may be a good idea to invest in some good probiotics. In particular, Butyric acid (4 carbon) saturated fatty acid is produced by several gut flora species and has favorable effects on our metabolism and protects against cancer.
Medium chain triglycerides (particular 6-12 carbon fatty acids) of which Lauric acid (12) is an example are extremely beneficial for health. Coconut oil and other coconut products contain a lot of MCTs specifically Lauric acid (66%). MCTs are useful for a variety of reasoning including weight loss -- increases oxidation of fatty acids, increases HDL-cholesterol (e.g. the "good" one), anti-bacterial, anti-oxidant, and is anti-inflammatory.
Most types of animal products have some combination of the long chain triglycerides which include the aforementioned Myristic acid, Palmitic acid, and Stearic acid. Each of these have slightly different effects on the body.
All excess energy in the body is specifically converted into palmitic acid, which will make up the majority of the "triglycerides" that you see in a blood panel. Fructose sugar in particular, is a toxin in the body. When it enters the body through the digestive tract, the liver must convert it into a usable form of energy. The energy form that it is converted into palmitic acid -- a saturated fatty acid.
Cholesterol
Cholesterol is a very, very, very important substance in the body. Cholesterol is in every cell of the body and helps to maintain the fluidity of the cell membranes, and regulation of substances passing through them. Additionally, it is intimately involved in nervous system regulation and makes up a large portion of the myelin sheath that speeds up nerve conduction in the body. Additionally, cholesterol is the backbone on which steroid hormones such as testosterone, estrogen, progesterone, etc. are created, and it is also a precursor to vitamin D as sun is required to photo-convert 7-dehydro-cholesterol into proto-vitamin D. Cholesterol is utilized in the adrenal glands to make cortisol and aldolsterone which help regulate fight-or-flight response, and sodium content in the body. Also, cholesterol is converted in the liver into bile salts which the gallbladder emits to help emulsify fatty acids and absorb many of the fat soluble vitamins -- A, E, D, K -- from dietary sources.
The transport of...
Since cholesterol is a hydrophobic substance, it cannot be transported in the body as it would stick to the vessel walls. Thus, the body creates HDL and LDL which are are lipoproteins (e.g. high density lipoprotein and low density lipoprotein) to transport cholesterol in the blood stream. Lipoproteins are composed of fat and protein. The "fatty" part binds to cholesterol so it can carry it, and the protein portion of it is hydrophilic so it can be dissolved into the blood until it gets to where the body needs it.
HDL carries cholesterol back to the liver, LDL carries cholesterol away from the liver to other tissues.
Lipid panels
So let's talk lipid panels.
When you see LDL and HDL in a blood panel it refers to how much LDL there is, and how much HDL there is.
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Total cholesterol level -- total cholesterol is technically a misnomer since it is a summation of all of the components of lipids in the blood sample (e.g. what a typical blood stream of someone looks like it). It isn't just total "cholesterol" which would just be a summation of HDL and LDL.
Triglyceride level -- triglycerides represent the amount of fatty acids -- palmitic acid mostly -- that is circulating in your blood stream. Triglycerides are the primary source of energy in the body, especially during aerobic exercise. Glucose is only primarily utilized at anaerobic threshold or above.
HDL cholesterol -- represents the amount of HDL in the body.
LDL cholesterol -- represents the amount of LDL in the body. There's actually lots of different subclasses of LDL proteins which a typical lipid panel won't show. Specifically, oxidized LDL (oLDL) or specifically Apolipoprotein B (or ApoB for short) is extremely strongly correlated with the development of cardiovascular disease. Apo B is sometimes referred to as small, dense LDL.
Therefore, you may have high LDL, but if you have a lot of "fluffier" LDL you are at a relatively low risk for cardiovascular disease. If you have low LDL but a lot of the "small, dense" oLDL / ApoB then you are at high risk for CVD. This is why it is important to get LDL subclasses checked even though most doctor's don't know this.... LDL matters little if you don't know if you have the big, fluffy or the small, dense.
There's actually three other classes of lipoproteins that carry fats in the body. Chylomicrons carry triglycerides from the digestive tract into the body. VLDL (very low density lipoprotein) and IDL (intermediate density lipoprotein) also carry fatty acids, but typically these aren't measured.
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Why are these supposed to be bad?
HDL, LDL, Cholesterol, triglycerdies, etc are neither "good" or "bad." They are needed in the body for various purposes. Only when they get out of whack does it means something is wrong.
According to the lipid hypothesis, high triglycerides and high LDL and low HDL are supposed to contribute towards heart disease.
Picture of atherosclerotic development
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The development of atherosclerotic lesions show increased fatty accumulations including cholesterol filtrates at the site of the lesion. Sounds correct, right?
Therefore, if you can prove that if high dietary fat intake -- especially saturated fats -- (1) raises blood lipids and (2) increases rates of atherosclerosis then it would be a cause and effect relationship.
Is it cause and effect? Or is it something else.
The chronic endothelial dysfunction theory better fits the data, especially in conjunction with nutritional studies regarding low carbohydrate versus low fat diets. It's funny but every time I browse the literature, there are only good results from low carbohydrate (which include "high fat" and "high protein") diets as opposed to low fat diets.
For example, this mayoclinic study says:
http://www.mayoclinicproceedings.com/content/78/11/1331.full.pdfEffect of a High Saturated Fat and No-Starch Diet on Serum Lipid Subfractions in Patients With Documented Atherosclerotic Cardiovascular Disease
• Results: In patients with atherosclerotic cardiovascular disease, mean ± SD total body weight (TBW) decreased 5.2%±2.5% (P<.001) as did body fat percentage (P=.02). Nuclear magnetic resonance spectroscopic analysis of lipids showed decreases in total triglycerides (P<.001), very low-density lipoprotein (VLDL) triglycerides (P<.001), VLDL size (P<.001), large VLDL concentration (P<.001), and medium VLDL concentration (P<.001). High-density lipoprotein (HDL) and LDL concentrations were unchanged, but HDL size (P=.01) and LDL size (P=.02) increased. Patients with polycystic ovary syndrome lost 14.3%±20.3% of TBW (P=.008) and patients with reactive hypoglycemia lost 19.9%±8.7% of TBW (P<.001) at 24 and 52 weeks, respectively, without adverse effects on serum lipids.
Lipid panels improved on almost every measurable and patients lost weight on a high fat no starch diet. And they had cardiovascular disease. So basically, this diet improved their cardiovascular disease.
Take for example, this non-biased search boolean on low carbohydrate vs. low fat:
http://scholar.google.com/scholar?q=low carbohydrate low fatThe first study suggests:
http://www.nejm.org/doi/full/10.1056/NEJMoa022637Severely obese subjects with a high prevalence of diabetes or the metabolic syndrome lost more weight during six months on a carbohydrate-restricted diet than on a calorie- and fat-restricted diet, with a relative improvement in insulin sensitivity and triglyceride levels, even after adjustment for the amount of weight lost.
This finding should be interpreted with caution, given the small magnitude of overall and between-group differences in weight loss in these markedly obese subjects and the short duration of the study. Future studies evaluating long-term cardiovascular outcomes are needed before a carbohydrate-restricted diet can be endorsed.
Of course, they ended with the cautioning, but there are many other studies.
The second study suggests:
http://jcem.endojournals.org/content/88/4/1617.full?l=5579341The very low carbohydrate diet group lost more weight (8.5 ± 1.0 vs. 3.9 ± 1.0 kg; P < 0.001) and more body fat (4.8 ± 0.67 vs. 2.0 ± 0.75 kg; P < 0.01) than the low fat diet group. Mean levels of blood pressure, lipids, fasting glucose, and insulin were within normal ranges in both groups at baseline. Although all of these parameters improved over the course of the study, there were no differences observed between the two diet groups at 3 or 6 months. β- Hydroxybutyrate increased significantly in the very low carbohydrate group at 3 months (P = 0.001). Based on these data, a very low carbohydrate diet is more effective than a low fat diet for short-term weight loss and, over 6 months, is not associated with deleterious effects on important cardiovascular risk factors in healthy women.
So they are similar.... oh wait, but hey we didn't look at the study's methods.
Subjects were randomized to 6 months of either an ad libitum very low carbohydrate diet or a calorie-restricted diet with 30% of the calories as fat.
So the low carbohydrate high fat diet did just as well as a calorie restricted lower fat diet. Why didn't they restrict kcals for the high fat diet too? Wouldn't that make a difference as well?
The third study suggests:
http://www.annals.org/content/140/10/769.shortResults: A greater proportion of the low-carbohydrate diet group than the low-fat diet group completed the study (76% vs. 57%; P = 0.02). At 24 weeks, weight loss was greater in the low-carbohydrate diet group than in the low-fat diet group (mean change, −12.9% vs. −6.7%; P < 0.001). Patients in both groups lost substantially more fat mass (change, −9.4 kg with the low-carbohydrate diet vs. −4.8 kg with the low-fat diet) than fat-free mass (change, −3.3 kg vs. −2.4 kg, respectively). Compared with recipients of the low-fat diet, recipients of the low-carbohydrate diet had greater decreases in serum triglyceride levels (change, −0.84 mmol/L vs. −0.31 mmol/L [−74.2 mg/dL vs. −27.9 mg/dL]; P = 0.004) and greater increases in high-density lipoprotein cholesterol levels (0.14 mmol/L vs. −0.04 mmol/L [5.5 mg/dL vs. −1.6 mg/dL]; P < 0.001). Changes in low-density lipoprotein cholesterol level did not differ statistically (0.04 mmol/L [1.6 mg/dL] with the low-carbohydrate diet and −0.19 mmol/L [−7.4 mg/dL] with the low-fat diet; P = 0.2). Minor adverse effects were more frequent in the low-carbohydrate diet group.
So higher retention rate with low carbohydrate. Check. Greater weight loss with low carbohydrate. Check. Low carb decreased serum triglycerides more. Check. Low carb diet increases HDL more. Check. Not sure what the minor adverse effects were, but they sure weren't big enough to have the retention rate go down more than the other group.
So I checked to at least 20 of the top results and low carbohydrate is at least equally or more effective than low fat diets (when compared) at both losing weight and on markers of cardiovascular disease risk. Check them out if you don't believe me.
Meta studies such at this one show similar findings.
http://onlinelibrary.wiley.com/doi/10.1111/j.1467-789X.2008.00518.x/fullThere are few studies comparing the effects of low-carbohydrate/high-protein diets with low-fat/high-carbohydrate diets for obesity and cardiovascular disease risk. This systematic review focuses on randomized controlled trials of low-carbohydrate diets compared with low-fat/low-calorie diets. Studies conducted in adult populations with mean or median body mass index of ≥28 kg m−2 were included. Thirteen electronic databases were searched and randomized controlled trials from January 2000 to March 2007 were evaluated. Trials were included if they lasted at least 6 months and assessed the weight-loss effects of low-carbohydrate diets against low-fat/low-calorie diets. For each study, data were abstracted and checked by two researchers prior to electronic data entry. The computer program Review Manager 4.2.2 was used for the data analysis. Thirteen articles met the inclusion criteria. There were significant differences between the groups for weight, high-density lipoprotein cholesterol, triacylglycerols and systolic blood pressure, favouring the low-carbohydrate diet. There was a higher attrition rate in the low-fat compared with the low-carbohydrate groups suggesting a patient preference for a low-carbohydrate/high-protein approach as opposed to the Public Health preference of a low-fat/high-carbohydrate diet. Evidence from this systematic review demonstrates that low-carbohydrate/high-protein diets are more effective at 6 months and are as effective, if not more, as low-fat diets in reducing weight and cardiovascular disease risk up to 1 year. More evidence and longer-term studies are needed to assess the long-term cardiovascular benefits from the weight loss achieved using these diets.
Honestly, how much data do you need to accumulate to prove that "high fat" diets do not cause cardiovascular disease. Saturated fat, and cholesterol don't cause cardiovascular disease.
So going back to specifically something like eggs which have a bunch of cholesterol and fat in them:
http://www.ncbi.nlm.nih.gov/pubmed/22037012http://www.ncbi.nlm.nih.gov/pubmed/20683785http://www.ncbi.nlm.nih.gov/pubmed/18991244http://www.ncbi.nlm.nih.gov/pubmed/21776466http://www.ncbi.nlm.nih.gov/pubmed/19369056http://www.ncbi.nlm.nih.gov/pubmed/21134328http://www.ncbi.nlm.nih.gov/pubmed/15164336http://www.ncbi.nlm.nih.gov/pubmed/18991244http://www.ncbi.nlm.nih.gov/pubmed/18203890http://www.ncbi.nlm.nih.gov/pubmed/17531457http://www.ncbi.nlm.nih.gov/pubmed/16340654The evidence vindicates saturated fats risk on heart disease.
http://wholehealthsource.blogspot.com/2011/01/does-dietary-saturated-fat-increase.htmlhttp://www.ajcn.org/content/early/2010/01/13/ajcn.2009.27725.abstracthttp://www.ajcn.org/content/80/5/1175.full.pdf html <-- decreased risk in post menopausal women with increased sat fat intake
http://healthydietsandscience.blogspot.com/2011/03/high-saturated-fat-diet-gives.htmlhttp://www.mayoclinicproceedings.com/content/78/11/1331.full.pdfetc.
In the same line this is why whole milk is healthier than skim milk:
http://wholehealthsource.blogspot.com/2010/12/dairy-fat-and-diabetes.htmlhttp://www.ncbi.nlm.nih.gov/pubmed/16904009http://www.ncbi.nlm.nih.gov/pubmed/20372173http://www.ncbi.nlm.nih.gov/pubmed/17925824http://www.ncbi.nlm.nih.gov/pubmed/11350992Another interesting article that was ahead of its time:
http://www.sciencedirect.com/science/article/pii/S0002934396004561So I hate to beat the drum on things I've already covered but the lipid hypothesis really does not make sense when you look at the literature.
When you find studies that support the role of fats in the development in cardiovascular disease and look at some of the specifics of the diet they ate they usually contain large amounts processed fats such as trans fats (which are notoriously bad for you).
This is to say that NORMAL sources of fats and oils such as animal fats, eggs, milk, butter, etc. are good for you. Industrial processed fats such as margarine, deep fried foods, vegetable oils, etc. in general are bad for you.
So what actually causes cardiovascular disease if it's not saturated fats and cholesterol?
Remember what I said before about lipid profiles?
They indicate something is wrong but they don't indicate what is wrong. The lipid hypothesis takes the incorrect step of saying that the lipids themselves cause the problems.
So that leaves us with the chronic endothelial injury hypothesis.
What likely happens is multifold.
1. Dietary effects of high carbohydrate diets (especially fructose) lead to increases in oxidized LDL. Oxidized LDL can get "stuck" in the endothelial wall which aggravates the tissues. The body sends macrophages to help try to clean up the damage. Inflammation results and the chain reaction continues.
2. Ingestion of large amounts of carbohydrates (especially fructose) lead to increases in advanced glycated end products. Fructose is 9x more likely than glucose to form AGE's by the way.
3. Trans fats.
4. Omega 3 vs Omega 6 fatty acids. Normal ancestral consumption in about 1:1 or 1:2 ratio. Normal consumption now is in 10:1 to 20:1 or higher ratios, especially in fried foods.
5. Dysregulation/dysfunction of the body's systems.
Leptin resistance contibutes to obesity. High carbohydrate/sugar intake contributes to metabolic syndrome and weight gain. All of these contribute to insulin resistance. Insulin resistance starts to contribute to dyslipedemia. You get obese, diabetes, high blood pressure, poor lipid panels. Then you get cancer, stroke, heart attack, etc.
http://en.wikipedia.org/wiki/Fructose#Health_effectshttp://en.wikipedia.org/wiki/Non-alcoholic_fatty_liver_diseasehttp://en.wikipedia.org/wiki/Metabolic_syndromeIf you are obese or have documented cardiovascular disease et al. you should know that some of the disease can be reversed to an extent with a low carbohydrate, ketogenic, or Paleolithic diet.
EPT
what with their tofu and meat-replacement stuff...
