Dr. Anthony Rosenzweig says his mice prove low-carb bad for the heart
In September 2009, my brand new book 21 Life Lessons From Livin’ La Vida Low-Carb: How The Healthy Low-Carb Lifestyle Changed Everything I Thought I Knew is slated to be released at long last (YEAH!) and I am excited to be able to share so much of the knowledge I have gleaned from personal research and interviewing experts about diet, health, and life in general over these past five years of living the low-carb life. Looking at Lesson #19 of my book, it says “You can’t always trust or believe the negative studies on low-carb.” How timely because there’s a perfect example of this appearing all across the media today with so-called damning research about how a low-carb diet negatively impacts vascular health. Hoo boy!
In a study entitled “Vascular effects of a low-carbohydrate high-protein diet,” lead researcher Dr. Anthony Rosenzweig, Director of Cardiovascular Research in Beth Israel Deaconess Medical Center’s Cardiovascular Institute and Professor of Medicine at Harvard Medical School, and his research team observed over a 12-week period a mouse model of atherosclerosis (plaque accumulation in the arteries leading to the heart–a precursor for a heart attack or stroke) and fed them one of three isocaloric diets with various fat/protein/carbohydrate ratios:
GROUP 1 — standard mouse “chow” diet (15/20/65)
GROUP 2 — a typical “Western diet” (42/15/43)
GROUP 3 — low-carb, high-protein diet (43/45/12)
Okay, hang on a sec. Before we even get into what Dr. Rosenzweig found in this study, let’s take a look at the diet they are using for this “low-carb” group. While it is indeed low in carbohydrate comprising just 12 percent of the total caloric intake, what’s up with the astronomically high protein content? Most of the reputable low-carb plans out there such as Atkins, Protein Power, and the like are decidedly much higher in FAT (upwards of 70 percent of total calories coming from fat) with only moderate or adequate amounts of protein. A 45 percent protein low-carb diet is nothing at all like what so many of us who are livin’ la vida low-carb would be consuming following a typical low-carb diet.
With that one caveat aside for now, let’s take a closer look at what the researchers did with these mice. They examined them at the six-week and twelve-week mark to see what impact had been made on the various study groups. Weight gain in mice is expected, but GROUP 3 gained 28 percent LESS weight than GROUP 2 — not a surprising result since most scientists acknowledge previous research showing the effectiveness of low-carb diets for weight loss. But when they looked at the blood vessels of the GROUP 3 mice, the researchers found that plaque build-up was nearly double (15.3%) than what GROUP 2 experienced (8.8%). GROUP 1 showed little evidence of atherosclerosis by comparison.
The researchers expressed concern that HUMANS consuming a high-protein, low-carb diet like the one consumed by these mice would lead to an inability to get the proper blood flow to the heart which could result in a cardiovascular event. Interestingly, the study found that the lipid profile of the GROUP 3 mice remained unchanged despite the supposed damage done to the blood vessels. This study was published in the August 24, 2009 online version of Proceedings of the National Academy of Sciences.
What’s my initial reaction to such a study that attempts to put livin’ la vida low-carb in a bad light? I SURE AM GLAD I AIN’T A MOUSE USED IN THIS STUDY! Seriously, are they for real? While mice can certainly be used in certain laboratory experiments to see what would happen to people in similar situations, I am not seeing the connection between a mouse and a human in this “study.” In fact, Nutrition & Metabolism founder and editor Dr. Richard Feinman responded to this discrepancy by noting “the scientifically correct title of this study should be ‘Vascular effects of a low-carbohydrate high-protein diet in ApoE mice’ because that is what it is about.”
Noted Milwaukee, WI-based cardiologist Dr. William Davis added another wrinkle to this study by revealing to Livin’ La Vida Low-Carb that “there are three forms of ApoE mice (2,3,4), each of which responds differently to different diets. For example, apoE2 people (and mice) respond to low-fat diets differently than apoE4 people.” Now this is getting really interesting. So which mice did Dr. Rosenzweig and his team use? It’s anyone’s guess!
Good Calories, Bad Calories author Gary Taubes explained to Livin’ La Vida Low-Carb that this study using mice actually contradicts a great preponderance of the evidence that we’ve already seen in human studies, including how an Atkins low-carb diet improves cholesterol panels, reduces inflammation, lowers blood pressure and more. So why are mice a better model for the development of atherosclerosis in humans than humans? Excellent question, Gary!
Although Dr. Rosenzweig admits it is “very difficult” to know how a diet is truly impacting cardiovascular health even in clinical studies, he insists that using mice fills in the gaps and answers the most pressing questions.
“We, therefore, tend to rely on easily measured serum markers [such as cholesterol], which have been surprisingly reassuring in individuals on low-carbohydrate/high-protein diets, who do typically lose weight,” he stated. “But our research suggests that, at least in animals, these diets could be having adverse cardiovascular effects that are not reflected in simple serum markers.”
Okay, let me get this straight to make sure I am understanding you correctly, Dr. Rosenzweig. Are you saying the improvements low-carb dieters in human studies have seen time and time again in their cholesterol, including increases in HDL “good” cholesterol, significant decreases in triglycerides, and an increase in the size of the LDL particles to the large, fluffy, and protective kind, are actually irrelevant as a true indicator of heart health because your mice happened to show negative cardiovascular effects even with all these improved markers? In other words, are we just supposed to chunk all that previous data that shows otherwise and simply believe the mice in your study hold the key to truly understanding what a low-carb nutritional approach is doing in humans? I DON’T THINK SO!
I’m gonna offer up a human case study that demonstrates how low-carb does NOT lead to plaque build-up in the arteries leading to the heart and it in fact does just the opposite.
A 37-year old male who has been eating a high-fat, moderate-protein, low-carb diet for 68 months had a CT scan of his chest conducted last week to see if there were any calcium deposits in the arteries leading to his heart. This heart scan as advocated by Dr. Davis would show any calcification of the plaque that has taken place as a result of his diet and assign a number to indicate the overall risk to cardiovascular problems. When the test results came back from this long-term low-carb eater, they showed his heart scan calcium score was zero. Despite eating a low-carb diet just as these mice did in this study, there was no calcified plaque at all.
By the way, the man featured in this case study is me, Jimmy Moore. WOO HOO!
Dr. Rosenzweig is probably not impressed by my phenomenal heart scan results attributed to low-carb living since he seems to be hedging all of his bets on mice. But the anti-low-carb bias is not just limited to him — another one of the researchers on this study named Dr. Shi Yin Foo, a cardiologist at Rosenzweig’s lab, claims that she wanted to do this study when several of her heart attack patients claimed to be livin’ la vida low-carb. In fact, Dr. Rosenzweig was also eating low-carb at the time which came as a shock to Dr. Foo.
“Over lunch, I’d ask [Dr. Rosenzweig] how he could eat that [low-carb] food and would tell him about the last low-carb patient I’d admitted to the hospital,” Dr. Foo exclaimed. “[Dr. Rosenzweig] would counter by noting that there were no controls for my observations.”
That was one of the reasons why they decided to concoct this mouse experiment “so that we could know what happens in the blood vessels and so that I could eat in peace,” Dr. Rosenzweig said.
Dr. Foo believes the diet composition they came up with most closely matches “a typical low-carb diet.”
“In order to keep the calorie count the same in all three diets, we had to substitute a nutrient to replace the carbohydrates. We decided to substitute protein because that is what people typically do when they are on these diets,” he explained.
Uhhh, no it isn’t, Dr. Foo! Most people who have read a reputable book on low-carb dieting knows that when you remove the carbohydrate you replace it with an increase in the percentage of fat in the diet. Generally it’s not a significant increase in the amount of dietary fat consumed since combined with a reduction in carbs and an adequate amount of protein this way of eating is quite satiating. But knowledgeable low-carbers are abundantly aware of the excessive glucose that comes from eating too much protein (through the process known as gluconeogenesis). And 45 percent of calories from protein is way too much by as much as DOUBLE! I regularly get only about 20-25 percent of my calories from protein and my fat intake is a whole lot higher than 43 percent.
University of Connecticut researcher Dr. Jeff Volek, who has conducted numerous studies on low-carbohydrate diets, told Livin’ La Vida Low-Carb that “no reasonable person would replace carbs with protein to the level these mice consumed.” He added that “mice are horrible models of lipoprotein metabolism and atherosclerosis…because regular mice are resistant to atherosclerosis.”
The researchers expressed shock that all of the typical markers for cardiovascular disease such as cholesterol, triglycerides, oxidative stress, insulin and glucose all came back normal for the low-carb GROUP 3 mice.
“In each case, there was either no difference in measurements compared with the mice on the Western Diet [which contains the same amount of fat and cholesterol] or the numbers slightly favored the low-carb cohort,” Dr. Foo added. “None of these results explained why the animals’ blood had more atherosclerotic blockages and looked so bad.”
Oh, boo hoo, woe is me for ever thinking of going on a low-carb diet! I had no idea things could be so bleak even though all my health markers have been spectacular. Don’t you know this study is being set up purposely to respond to low-carbers who have outstanding cholesterol, triglycerides, blood sugar and insulin levels as if to say, “Sure, your blood works comes back clean, but we REALLY know what is happening to your arteries!” Do they really think we’re that stupid?
Well, for Dr. Rosenzweig, the results of this study were enough to have him cease with his healthy low-carb way of eating.
“Examinations of the animals’ bone marrow and peripheral blood showed that the measures of EPC cells dropped fully 40 percent among the mice on the low-carb diet – after only two weeks,” he remarked. “Although the precise nature and role of these cells is still being worked out – and caution is always warranted in extrapolating from effects in mice to a clinical situation – these results succeeded in getting me off the low-carb diet.”
Dr. Volek notes that a better animal model for conducting a study like this would have been guinea pigs which he says would “have shown low carbohydrate diets decrease cholesterol accumulation and inflammation in the aorta.” And he added that his own research of low-carb diets in humans has shown “in the same 12 week period…that humans consuming low carbohydrate diets have increased vascular function.”
Dr. Davis also chimed in that this study doesn’t jive with what he’s seen.
“I cannot reconcile what this study says with what I see in clinical practice: Low-carb diets yield not only extravagant weight loss, but also marked reductions in triglycerides, small LDL, blood pressure, blood sugar, reversal of pre-diabetic patterns and even diabetes, and is associated with reductions in CT heart scan scores,” he noted.
When Livin’ La Vida Low-Carb asked Kansas low-carb diet practitioner Dr. Mary C. Vernon about this, she quickly concurred with Dr. Davis in her trademark matter-of-fact way of saying things.
“This study just doesn’t fit with what I have seen in patients. I have had patients with pre-existing coronary disease who should have had worsening of their artery blockage have no advancement of their disease when they had repeat cardiac catherization,” she explained. “To have no advancement of disease is unheard of in patient’s treated the standard way in the United States. I have seen patients with high levels of protein leaking from their kidneys return their kidney function to normal. And here is a twist –the diet people are taught to eat after bariatric surgery ends up being a low-carb one. So where is all the accelerated atherosclerosis in those patients?”
What is the take-home message the researchers want to leave with people?
“For now, it appears that a moderate and balanced diet, coupled with regular exercise, is probably best for most people,” they concluded.
Well, how very convenient for you to come to this conclusion! But this little study of yours is absolutely irrelevant because it fails to acknowledge all the previous HUMAN studies that come to the exact OPPOSITE results. If you had a choice between believing a study of mice or a study of humans regarding your heart health, then which one would be more convincing to you? Obviously it’s the human one. And there are plenty of human studies out there that could have been cited by these researchers — but they didn’t do it! As Dr. Feinman explained to Livin’ La Vida Low-Carb, “For them not to cite papers that contradict their findings is dishonest.”
One of my readers shared with me regarding this study the fact that mice are herbivores and, as he put it so succinctly, “may lack the physiological mechanisms to transport and utilize proteins and fatty acids as an energy alternative to glucose” compared with humans. In other words, the diet fed to these mice is very likely unnatural “if the creatures were forced to eat something they cannot metabolize, or metabolize poorly.”
This is something Dr. Vernon expressed concern about as well.
“Someone with more mouse knowledge than I have needs to address the mouse chow composition,” she retorted. “What chow requirements are needed to produce nutritional ketosis in mice? Mice just don’t generally eat this way. How do the researchers know that the change in the mice is from the decrease in carbohydrate? Maybe the mice don’t tolerate the increase in protein in the study diet.”
Dr. Vernon added that it is a great leap of faith to extrapolate human comparisons with these irregular mice diet models — human study participants are necessary to confirm or reject the findings in the animals.
“I would never plan my diet around what makes a mouse healthy — rodents just aren’t very good models for humans. Of course, they reproduce rapidly and they make inexpensive research subjects, so a lot of research is done on mice. But follow-up studies using animals more like humans or humans themselves is needed before conclusions are reached,” she expressed.
My reader went on to give the example of a carnivore like a tiger whose primary diet is fat and protein and imagined what would happen if the animal were to be fed a higher percentage of carbohydrate than normal. Would he be “healthier” than his fellow tigers? Not likely! But isn’t this exactly what the researchers from Beth Israel have done with these mice? It’s a fascinating thing to think about and pokes holes in what is unfortunately being promoted as a reputable study.
Dr. Vernon says she welcomes more research on this, but she will always be more apt to respond to the improvements she has been seeing in her patients over the years.
“I monitor my patients closely, because I know that each individual is unique and may demonstrate a response that I have not seen before. In that case, I would see advancing vascular disease. I haven’t seen it yet, but I will continue to look for it,” she said. “This is why I think doctors need to be involved in nutrition — because this nutritional intervention is as potent as many of the drugs we use and it treats the problem at the source rather than symptom without addressing the cause of the problem.”
Dr. Volek summarized this so-called study in a pithy, yet thorough response.
“Let’s put this paper into context – it used an unsuitable animal model to study the effects of a diet no one would consume and showed results opposite to that seen in a more suitable animal model and humans,” he stated.
Is there anything else left to say after that? Feel free to share your comments below. Or better yet, let Dr. Rosenzweig know what you think about his mouse study by e-mailing him at arosenzw@bidmc.harvard.edu. Releasing research like this and extrapolating human application is irresponsible and unethical if you ask me. Researchers like him should know better!
What a waste of time this so-called researcher puts us through -if he had read Gary Taubes (Good Calories, Bad Calories) and Barry Groves (Trick and Treat) and what they had to say about experiments like this on rabbits early in the 20th century which, like mice, are not carnivores, and what implications it had on the lipid hypothesis, he might have constructed a better expeimental design. Whatever.
I predict that next time we will see somebody arguing that eating “sugar only” makes us super athletic by citing how energetically hummingbirds flap their wings on their high carb diet. If it works for them, ergo, it must work for us.
Thanks for sharing this, I especially like the “tiger example”. It doesn’t get any more basic than that.
Marc
I e-mailed Dr. Rosenzweig the below message right after I read an article about his research. Here’s my message:
Dear Dr. Rosenzweig,
I read this article http://news.bbc.co.uk/2/hi/health/8218780.stm entitled Low carb diets ‘damage arteries’ and decided to contact you. Perhaps the below excerpt will reassure you that a high-fat diet is safe and healthy in the context of a biologically potent diet.
In my estimation, our modern food supply has been mechanically and chemically reconfigured to the point where it is not likely to supply enough of the biochemical factors required to properly process calories from any source. That’s why I grow much of my own food. In fact, I call what I do “extreme gardening” because I get extremely good results from mixing enormous amounts of composted organic material with my soil, sometimes to a depth of 30 inches. The topsoil surrounding my home is only 8 to 12 inches deep (and rather deplete because it was farmed for many years prior to being developed for housing) but plants will send their roots quite a few feet into the ground if the nutrients are there.
But enough of that. Here’s the excerpt from Nutrition Against Disease by Roger J. Williams, PhD, 1971.
“No discussion of heart disease would be complete without mention of the question of saturated fats. It has come to be almost an orthodox position that if one wishes to protect oneself against heart disease, one should avoid eating saturated (animal) fats. While this idea may not be entirely in error, it is misleading in its emphasis. The evidence shows that high fat consumption, when accompanied by plenty of the essential nutrients which all the cells need, does not cause atherosclerosis or heart disease.
Rats have been used extensively to study the effects of diet on atherosclerosis. Under ordinary dietary conditions the inclusion of saturated fats in their diet will consistently promote the deposition of cholesterol in their arteries.(50) For 285 days rats were fed a diet containing 61.6 percent animal fat, but highly superior with respect to protein, mineral, and vitamin content, without producing any pathological changes in the aorta or in the heart.(51) The animals did, to be sure, become obese, as much as three to four times their normal weight. Animals fed vegetable fats at the same level fared essentially no better and no worse. These findings were based upon extensive long-term experiments at Yale, using a total of 600 rats, which were observed for as long as two years. There were no findings suggestive that either high animal fat diets or high vegetable fat diets were conducive under these conditions to atherosclerosis.
That cardiovascular disease is not associated with high fat diets is also shown by comparison study of matched groups of twenty-eight railwaymen from North India and twenty-eight from Southern India.(53) The consumption of fats, mostly of animal origin, was ten times higher among the North Indians than the South Indians, but there were no significant differences between their lipid and cholesterol levels. Among the South Indian population, the incidence of heart disease is said to be fifteen times as high as among the North Indians where the fat content of the diet is ten times higher. Dietary factors are doubtless very important in connection with the incidence of heart disease, but fat is only one factor, and other dietary factors are considerably more important.
This is also corroborated by a study of 400 Masai men in Tanganyika.(54) In spite of the fact that the diet of these men is almost exclusively milk and meat (consumption of whole blood is relatively rare), both of which contain much fat and plenty of cholesterol, the cholesterol levels in the blood of the Masai are extraordinarily low, and there was “no evidence of arteriosclerotic heart disease.” It should be noted that a diet containing large quantities of meat is free from “naked calories,” and is certain to supply an assortment of amino acids, minerals, and vitamins in liberal amounts. Though the Masai have other health disorders – many of infective origin – they probably escape heart disease because their body cells are furnished with an environment that is adequate enough to protect their hearts and blood vessels.
A corollary of the notion that saturated fats are arch villains is the idea that one should eat substantial amounts of polyunsaturated fats. (The phrase “polyunsaturated fatty acids” has become virtually synonymous with “heart protection” in both popular and orthodox medical thinking.) While everyone should have unsaturated fats in his diet, their presence does not by any means afford adequate protection against atherosclerosis and heart disease. The current consumption of polyunsaturated fatty acids in the USA is higher than it has ever been, yet this does not curb heart disease.(55) There are many reasons on which to base our conclusion that other factors are far more important.(56) When other deficiencies are eliminated, the amount of unsaturated fat is of secondary importance. If there is plenty of vitamin B6 in the diet, fat metabolism tends to take care of itself.
I have said a good deal about vitamin B6, but I do not mean to imply that it is, by itself, the answer to heart disease. All the nutrients contribute to the prevention of heart trouble.”
Notes for the above excerpt are published on my blog at http://nutritionscienceanalyst.blogspot.com/2008/02/nutrition-against-disease.html .
Here’s a paragraph from the notes (54): “It is clear, therefore, that adult males of a widely differing ethnic stock can subsist on a high fat, high cholesterol, high caloric diet, and yet remain relatively free of cardiovascular disorders. Even if prevailing views are to the contrary, I think that the evidence points strongly toward the conclusion that the nutritional environment of the body cells – involving minerals, amino acids, and vitamins – is crucial, and that the amount of fat or cholesterol consumed is relatively inconsequential.”
Whether a diet emphasizes fat or carbohydrate, the important thing is to provide enough supportive nutrition to process the calories. The Kitava Study is an example of a high-carb diet that protects from heart disease. http://www.staffanlindeberg.com/TheKitavaStudy.html
I hope this information proves helpful.
Regards,
David Brown
1925 Belmar Dr
Kalispell, MT 59901
Ph/406-257-5123
Nutrition Education Project
Well done Dave, let us know if you get a reply.
Jimmy, another great critique. I suggest you take the good Dr Rozenzweig’s report, rip it up into small squares, thread with string and hang it up in the smallest room where it will be of some use.
Sometimes I think the ‘experts’ rely on us being ignorant so that they can pass off their bunk and we won’t know any different. Well they have met their match in an educated low carber.
Susie
THANKS Susie! I only wish I could have gotten this one into my new book.
–Jimmy
Well, the other obvious questions not answered (or at least addressed in your post) regard the diet of the mice. What was the source of the protien? Was it actually animal flesh, bugs, eggs, or soy, wheat, corn etc? And the same question with the fat – saturated fat? PUFA’s? Olive oil?
That data could put some interesting twists on the results, at least for mice breeders
We have no idea Lucy since the researchers didn’t provide this information. Another flaw.
–Jimmy
Jimmy, great analysis. I did not read the full study since I was not willing to pay for it, but when I read the abstract a couple days ago and saw the low-carb mice consumed 45% of their intake in protein my first thought was “huh?” That’s big boatload of protein. And when I read: “We decided to substitute protein because that is what people typically do when they are on these diets,” he explained.”
I said to myself, “Do these people really understand low carb diets at all?” As you said, most of us substitute fat for the missing carbs. I know I sure do! My typical protein intake is about 15-20% of my daily calories.
Of course low carb is not helping with weight loss any. I have 120+ pounds to lose and have not lost an ounce since the end of February (well yes I have, I constantly bounce up and down over the same 5-pound range) despite strict adherence to La Vida Low Carb. So I do get jealous of the things like “extravagent” weight loss seen by Dr. Davis – since it sure ain’t happening for me. I feel like there’s a big low carb party going on and I didn’t get an invitation.
Awww, Debbie, don’t get discouraged. There are other ways to measure success besides weight loss–are you healthier, do you feel better, and has your life changed at all in the positive direction since you started livin’ la vida low-carb? Those are the things to CELEBRATE, my friend. KEEP AT IT!!!
–Jimmy
Jimmy, that’s great about your heart scan, pretty hard to beat zero.
Also, I think it’s astounding that the American Heart Association says this week that people need to cut drastically down on their sugar intake. I’m not aware that they have ever before linked carbs and heart disease.
The other person I’ve heard of as having no plaque was Nathan Pritikin.
He died at age 70 after having had an extensive history of heart disease, but after years of his almost no fat diet, the person who did the autopsy told the press that his arteries were as clean as a baby’s. Be interesting to know what you and he have in common (even though obviously you have different theories of heart disease and different diets.)
Nathan Pritikin was riddled with leukemia. He committed suicide at age 69. Apparently, his leukemia had been in remission, but returned even after many years on his low-fat diet. (He was rabidly ant-fat, but also anti-sugar.)
http://en.wikipedia.org/wiki/Nathan_Pritikin
http://www.people.com/people/archive/article/0,,20090134,00.html
What’s an ApoE mouse? What’s an ApoE human?
ApoE (short for apolipoprotein E) is one of the protein components of the cholesterol and fat-carrying particles known as lipoproteins (LP) that circulate in the blood. It is required for efficient clearance of some of these particles. What should have been written in Jimmy’s article is ApoE knockout mice, that is, mice that have been genetically engineered to have no ApoE. Such mice are naturally prone to atherosclerosis because of the poor clearance of the LP particles. So the mice in this study were ApoE-KO mice (genetically referred to as ApoE-/-) which have to be used to study atherosclerosis (or more precisely the role of Apo-E) because normal mice don’t generally develop atherosclerosis possibly because of very high HDL.
It is rare for humans to be deficient in ApoE but those people who are, do have high cholesterol but I believe are not particularly susceptible to atherosclerosis.
Is this a good model for human lipid metabolism and the effect of low carbohydrate diets (LCD)? One suggestion that it is not is that the triglycerides went up on the LCD which almost never happens in humans when they reduce carbohydrates. One tries to be collegial in research but this work, or at least the authors interaction with the press, seems very biased and somewhat hostile and I am pretty much at a loss as to what to say.
they can produce studies till the cows come home, publish scathing media pretties for all to read. but the bottom line is, people are finding health by letting go of the lipid hypothosis. real humans, with real medical tests to prove what they already knew, they are benefiting and regenerating with more healthy fats, and dietary cholestorol finally being able to do its work and rebuild the cells. i love it when a “belief” is proven in the lab, and it has to become “fact”.
unless a persons preconcieved notions of reality are simply too entrenched in incoming grant money to be changed. some things are just too painful .
What I would REALLY like to know is not necessarily the ratios of the macronutrients (which, as Jimmy stated, absolutely nothing like a true low-carb healthy diet) but, rather, What the INGREDIENTS list looked like.
I am sure that it was not fresh meats and green veggies that’s for sure, but probably instead was powdered “egg” proteins, rancid or hydrogenated soy oils (or other rancid highly processed franken-oils).
Basically, I’m willing to bet that those mice were not fed REAL food at all, but “foods” that had been reduced to an unrecognizable form.
Sad….. really sad…..
There is one other small detail. The high carb diet did not have any added cholesterol while the low-carb and SAD diet had .15% (of energy) as added cholesterol. Feeding cholesterol to rats and other herbivore animals is a guarantee for atherosclerosis since they don’t have the same type of mechanism we (humans) have to clear cholesterol. Feeding saturated fat by itself does not create atherosclerosis in rats, rabbits, etc. Take a look at these studies:
Relative Failure of Saturated Fat in the Diet to Produce Atherosclerosis in the Rabbit
http://circres.ahajournals.org/cgi/content/abstract/20/6/658
Saturated fat without cholesterol = no atherosclerosis. Saturated fat + cholesterol = atherosclerosis
Effect of high fat diet without cholesterol supplementation on oxidative stress and lipid peroxidation in New Zealand white rabbits.
http://www.ncbi.nlm.nih.gov/pubmed/20032571
Effect of palm olein oil in a moderate-fat diet on plasma lipoprotein profile and aortic atherosclerosis in non-human primates.
http://www.ncbi.nlm.nih.gov/pubmed/12492629
Comparison between the effects of dietary saturated (16:0), monounsaturated (18:1), and polyunsaturated (18:2) fatty acids on plasma lipoprotein metabolism in cebus and rhesus monkeys fed cholesterol-free diets.
http://www.ncbi.nlm.nih.gov/pubmed/1728820
Thankfully, humans can deal with dietary cholesterol since we evolved eating cholesterol-containing foods.