The Effects of 15 days of 100 Grams of Saturated Fat Per Day on Cholesterol Levels in a healthy adult male.
By: Bryan Stell: BS West Chester University PA Exercise Science/Nutrition
Objective: It is widely believed that saturated fat in the diet increases blood cholesterol levels, promotes poor health as well as the progression of heart disease and atherosclerosis. The goal of this experiment is to compare pre and post bloodwork following 15 days of ~100g/saturated fat consumption per day to determine if there is any merit in this widely held belief.
Introduction: Saturated fat and cholesterol have long been avoided in the diet due to their believed link to heart disease and atherosclerosis. When saturated fat crosses the lips, some ignorant fool may shout " OMG, Yer gonna have a heart attack!" Or, "that bacon is clogging your arteries." For some 50 years food marketers and pharmaceutical companies have perpetuated these ideas, even though science is demonstrating that total cholesterol is an awful predictor of coronary heart disease (CHD) and that total LDL cholesterol or "bad" cholesterol is not much better. Furthermore, the entire case against saturated fat is inextricably linked to the idea that high cholesterol causes heart disease and that saturated fat in the diet increases blood cholesterol levels.
The USDA's 2010 dietary guidelines continue with the vilification of saturated fats by recommending they make up no more than 7% of one's daily caloric intake. This is down from a previously recommended upper limit of 10%. Instead they recommend replacing saturated fats with more mono-unsaturated and poly-unsaturated fats as well as carbohydrates. *Even though polyunsaturated fats (vegetable oils) lower HDL (good cholesterol), cause inflammation, and perhaps cancer (14). Furthermore, the governments recommendation for replacing saturated fats with a higher carbohydrate intake can exacerbate the atherogenic dyslipidemia associated with insulin resistance and obesity, increased triglycerides, small LDL particles (the "bad-bad" cholesterol) and reduced HDL ((the "good" cholesterol)16), especially if the carbohydrates are the refined variety.
It hasn't always been this way. Saturated fats where once a staple of a healthy diet. Our paleolithic ancestors prized animal fat and would preferentially consume it over leaner animal tissue(1). Our great grandfathers and their grandfathers would enjoy cholesterol rich foods such as eggs and bacon daily without thinking twice about their arteries clogging.
Methods: The 15 day test took place from Monday, June 20th to Tuesday, July 4th, 2011. The subject was a healthy 167 pound, 24 year old male. Bloodwork was drawn at around 11 AM after a full 8-9 hour night of sleep for both pre and post bloodwork.
The subjects previous diet was a seemingly healthy 'paleo' diet high in fruits and vegetables, healthy animals, some nuts and an already higher than average saturated fat and cholesterol intake. Occasional ice-cream and booze would enter the diet. The subject was relatively active most days and engaged in strength training 3-5x per week. Three 12 hour nightshifts (7pm-7am) were completed per week in both the pre and post dietary intervention.
The blood tests compared cholesterol via a VAP cholesterol test. Testosterone and thyroid hormones were also checked pre-and post dietary intervention by Atherotech Incorporated.
The dietary intervention aimed at consuming a maintenance level of calories (estimated at 2800 kcal/day) as to not induce weight gain, while allowing the subject to reach the target goal of 100 grams of SFA (saturated fatty acids) per day. 100 grams of saturated fat per day is 900 calories and 625% more than the American Heart Associations recommended upper limit of 16 grams per day. During the experiment the subject did not track his calories, rather wrote down in detail all the foods consumed and the exact amounts. The goal was just to average 100 grams of saturated fat per day while eating to satiety. Often he reported eating above and beyond satiety in order to achieve the requisite SFA intake.
All food was to be minimally processed 'real' foods. Cholesterol consumption was also encouraged. The foods eaten consisted of the "culprits" in raising cholesterol and thus, according to the traditional medical professionals; causing atherosclerosis and increasing risk of heart disease. Such foods are both high in fats, saturated fats and cholesterol. The main foods consumed were bacon, eggs, ribs, sausage, grassfed ground beef, coconut oil, grassfed butter, coconut milk, 85% dark chocolate and macadamia nuts. The more saturated fat, the better.
Over the 15 days, average caloric intake was higher than expected at approximately 3112 kcal/day. Average saturated fat intake was 102 grams or 918 kcal/day. Carbohydrates averaged 97 grams per day or 388 kcal/day. The subject went from a morning fasted weight of 167 lbs. to 165.5 lbs. Most of this weight loss was water weight as when more carbohydrates entered back into the diet weight went back to 167 within a couple days. Shift work, exercise and supplementation was the same through the pre and post dietary interventions.
Results: Positive or Anti-atherogenic results:
Total LDL dropped from 111 to 106 mg/dl.
IDL dropped from 17 to 6 mg/dl.
HDL increased from 60 to 76 mg/dl.
HDL2 increased from 17 to 24 mg/dl.
HDL3 increased from 43 to 52 mg/dl.
Total VLDL decreased from 22 to 18 mg/dl.
VLDL3 decreased from 13 to 11 mg/dl mg/dl.
Triglycerides decreased from 100 to 66 mg/dl.
Non-HDL cholesterol decreased from 133 to 124 mg/dl.
Remnant lipoproteins IDL+VLD3 decreased from 30 to 19mg/dl.
Testosterone increased from 586 to 841 ng/dl.
Results: Negative or potentially atherogenic:
Total Cholesterol increased from 192 to 200 mg/dl.
Lipoprotein A increased from 6 to 8 mg/dl.
In summary, the ONLY negative blood marker found could be lipoprotein A, which is one of the "bad-bad" LDL cholesterols increased from 6-8 mg/dl. Total cholesterol did increase by 8 mg/dl but the overall picture of total cholesterol was by all accounts greatly improved. Most significantly, Testosterone increased ~70%, from 586-841 and triglycerides decreased 34%, dropping from 100 to 66. HDL also increased ~27%, from 60 to 76.
Trigylcerides to HDL ("the good cholesterol") ratio has statistically shown to be one of the most potent predictors of heart disease (17, 18), and also all cause mortality (19). A Harvard study found that people with the highest ratio of triglycerides to HDL had 16x the risk of heart attack as those with the lowest ratio. Furthermore, high triglycerides alone increased the risk by 3x. Triglycerides/HDL was found to be a better predictor of heart disease than HDL/LDL and certainly total cholesterol. So in terms of the triglyceride to HDL ratio:
- 2 or less is considered ideal
- 2-4 is at risk
- 4-6 high risk
- 6+ plan a funeral
Our subjects Triglyceride/HDL ratio pre-bacon rich diet was (100/60) or 1.6 which is considered ideal. Post SFA and cholesterol rich diet intervention his ratio improved to 66/76 or .87 which is better than ideal.
Discussion: Atherosclerosis is a form of arteriosclerosis where the blood vessel hardens from the accumulation of lipid-laden macrophages within the arterial wall. This leads to a formation of a lesion called a plaque. Atherosclerosis is a pathologic process that can affect the vasculature throughout the body resulting in poor blood flow to the affected tissues. It is the leading contributor to coronary artery and cerebrovascular disease (heart attack and stroke).
There remains considerable controversy as to the pathophysiology of atherosclerosis. Traditional medicine sticks with the cholesterol hypothesis which goes like this.
"If you eat too much food containing cholesterol and/or saturated fat, the level of cholesterol in your blood will rise. The excess cholesterol will be deposited in artery walls, causing them to thicken and narrow. In time this will block blood supply to the heart (and other organs) causing a heart attack or stroke."
Thus, cholesterol in the blood is the problem and lowering cholesterol is a desirable treatment to reduce your risk of heart attack and stroke.
The contrarian view is rather that cholesterol is being deposited into the artery wall to repair endothelial damage. Cholesterol is the building blocks of all new cells, thus is necessary to repair the damage. This view would suggest that cholesterol is not the problem; the problem is whatever is causing the endothelial damage.
The most widely accepted theory to date is that atherosclerosis is an inflammatory disease (2). It begins with injury to the endothelial cells that line artery walls (3). The injury progresses to a fatty streak, then a fibrotic plaque to a complicated lesion. The initial injury can be attributed to risk factors for atherosclerosis such as smoking, hypertension, elevated blood glucose (diabetes), increased LDL, decreased HDL, and inflammatory auto-immune diseases. Other risk factors include elevated CRP, increased serum fibrinogen, insulin resistance, oxidative stress, infection and periodontal disease.
Once the injury has occurred in the endothelium...
- The inflamed cells cannot make normal amounts of anti-thrombotic and vasodilating cytokines.
- Numerous inflammatory cytokines are released.
- Macrophages adhere to injured endothelium.
- These macrophages then release enzymes and toxic oxygen radicals (that oxidize LDL) and further damage the injured vessel.
- Growth factors are released which stimulate smooth muscle cell proliferation in the affected vessel. (4)
So according to the latest science in pathophysiology, the problem is not cholesterol, it is endothelial damage stemming from inflammation. So without inflammation, blood cholesterol is a rather benign substance, even LDL. The problem is that our environment and our diets present many pro-inflammatory opportunities.
Our standard American diet (SAD) promotes inflammation in three main ways.
- Our ratio of omega 6 to omega 3 is skewed in a pro-inflammatory way. Evolution prescribed a 1:1 to 3:1 ratio of these fatty acids while our SAD diets typically are in the range of 15:1 to 16.7:1 (5). Negative effects of this ratio include inflammation (which progresses a plethora of disease states), oxidization of LDL and inhibition of the anti-inflammatory benefits of omega 3 fatty acids.
- Our highly refined carbohydrate diets lead to inflammation via elevated blood glucose and insulin resistance(6).
- Food allergies and intolerances often from relatively novel such foods as dairy (lactose) and wheat (gluten) can elevate inflammation in various tissues in the body. (7,8).
Our SAD diet promotes inflammation and denounces a molecularly stable fat, saturated fat. Saturated fat which is stable in the body and during cooking resists oxidization better than other fats, particularly polyunsaturated fats (omega 3,6,9. This means less free radical damage in your body. Recall that LDL is not a problem until it is oxidized. Furthermore, there are various types of LDL cholesterol. The smaller denser LDL are more prone to oxidization. These are the "bad-bad" cholesterol. The larger bouyant LDL are less prone to oxidization. These are the "good-bad" cholesterol.
Since elevated blood glucose is toxic, our bodies in their infinite wisdom are smart enough to turn it into a more benign substance, fat. Excess carbohydrate is thus turned into fat (Trigycerides) in the liver. Furthermore, high carbohydrate diets are known to produce the "bad-bad' LDL cholesterol. (9)
Low carb high fat (LCHF) diets are shown to promote more large bouyant "good-bad" LDL cholesterol (10). High fat diets also increase HDL, a negative risk factor for heart disease (11). While high fat low carb diets significantly reduce triglycerides better than any drug on the market (12).
The results of this N=1 study may surprise the layperson, but are not surprising in light of the available science. High fat diets are known to raise both HDL, LDL and thus total cholesterol. With such epic proportions of fat, and saturated fat in this study, it was not surprising that HDL rose, but LDL dropping is surprising. Total cholesterol rose from 192 to 200 mainly because HDL jumped 16 ng/dl (from 60 t0 76) while LDL dropped from 111 to 106 ng/dl. Overall, the post-dietary intervention cholesterol level of 200 ng/dl had a much better lipid profile than the lower cholesterol at 192 ng/dl. This stands for further proof that total cholesterol is a rather meaningless risk factor for heart disease.
Further, all subfractions of HDL and LDL improved except for lipoprotein A (LPA) which went from 6 ng/dl to 8 ng/dl. This also was unexpected as lipoprotein A is one of the small dense more easily oxidizable forms of LDL that usually decrease with HFLC diets. Perhaps the carbohydrate intake ~97g/day was too high to benefit the LPA.
Most notably, the EPIC saturated fat consumption intervention resulted in a ~70% increase in testosterone (586 pre to 841 post). If the prior results of this study were not enough to exonerate saturated fat from its suggested implications with heart disease then we must add the fact that high testosterone is protective of the heart. Lower testosterone levels in men are associated with increased heart comorbidities (15). (Higher fat diets and specifically higher saturated fat diets have shown to correlate with increased testosterone (13). 15 days of EPIC saturated fat consumption may result in increased growth of muscle and hardness of the male organ as well as other benefits.
Conclusion: This N=1 pilot study concludes that this one healthy young male can consume inordinate amounts of saturated fatty acids while precipitating positive health outcomes. Further, males interested in increasing testosterone and reducing their risk of CHD and CVD may want to implement a similar dietary strategy of HFLC, particularly of the saturated variety. (of course check with your physician and monitor your health yada yada).
1.) Cordain L. Saturated fat consumption in ancestral human diets: implications for contemporary intakes. In: Phytochemicals, Nutrient-Gene Interactions, Meskin MS, Bidlack WR, Randolph RK (Eds.), CRC Press (Taylor & Francis Group), 2006, pp. 115-126.
2.) Hansson GK: Inflammation, atherosclerosis, and coronary artery disease, New England Journal of Medicine. 352: 1685-1695, 2005.
3. Packard RR, Libby P: Inflammation in atherosclerosis: from vascular biology to biomarker discovery and risk prediction, Clinical Chemisry. 54 (1): 24-38 2008.
4.) McCance, Kathryn L., and Sue E. Huether. Pathophysiology: the biologic basis for disease in adults and children. 6th ed. St. Louis, Mo.: Elsevier Mosby, 2009. Print.
Pre-Dietary Intervention Bloodwork
Post Dietary Intervention Bloodwork
