How LDL Cholesterol Becomes Atherosclerotic Plaque

Here’s an inter­est­ing arti­cle about how high lev­els of LDL cho­les­terol end up caus­ing ath­er­o­scle­ro­sis.

The body uses cho­les­terol for var­i­ous pur­pos­es, and it has a sys­tem for trans­port­ing cho­les­terol in the blood­stream. Like fat, cho­les­terol doesn’t dis­solve in water. To trans­port fat and cho­les­terol via the blood­stream, the body puts them in pack­ages called lipopro­teins. As the name sug­gests, a lipopro­tein con­tains fat­ty sub­stances (lipids) as well as some pro­tein.

Not only do fat­ty sub­stances like cho­les­terol fail to dis­solve in water, they float on top of it. That’s because they are less dense than water. They are also less dense than pro­tein. The lipopro­tein par­ti­cles that are largest and con­tain the most fat also have the low­est den­si­ty. The “bad” cho­les­terol that peo­ple talk about is low-den­si­ty lipopro­tein (LDL). These are lipopro­tein par­ti­cles that car­ry fat and cho­les­terol from the liv­er to the rest of the body. LDL is like a wheel­bar­row full of fat and cho­les­terol trav­el­ing from the liv­er to the rest of the body. In con­trast, high-den­si­ty lipopro­tein (HDL) picks up the cho­les­terol from the tis­sues and car­ries it back to the liv­er. HDL is like a most­ly emp­ty wheel­bar­row pick­ing up fat and cho­les­terol and tak­ing it back to the liv­er.

The arti­cle explains that cho­les­terol is always enter­ing and leav­ing the inti­mal lay­er of the arte­r­i­al wall. The cho­les­terol is brought in by LDL and is tak­en away by HDL. If the cho­les­terol is brought in faster than it leaves, it builds up to form a deposit called an athero­ma. The more LDL there is in the blood­stream, the faster the LDL par­ti­cles enter the wall of the arter­ies. The cho­les­terol is like­ly to build up into an athero­ma if there isn’t enough HDL to car­ry the cho­les­terol back out fast enough or if the LDL under­goes some chem­i­cal change with­in the wall of the artery before it can be removed. Here’s an arti­cle that explains the kinds of chem­i­cal changes that can occur to the LDL while its inside the arte­r­i­al wall.

Why does cho­les­terol build up in the inti­ma of the arte­r­i­al wall but not in oth­er kinds of tis­sue? It’s because the con­cen­tra­tion of LDL is far high­er in the arte­r­i­al inti­ma than in any oth­er tis­sue. The prob­a­ble rea­son for this high LDL con­cen­tra­tion is the fact that the arte­r­i­al inti­ma is not drained by lymph ves­sels. LDL par­ti­cles are small enough to leak through the gaps between the endothe­lial cells that pave the inner sur­face of the artery. Then, they can dif­fuse through­out the loose struc­ture of the arte­r­i­al inti­ma. How­ev­er, they are too big to leak through the pores in the car­bo­hy­drate-and-pro­tein mesh­work of the medi­al lay­er. Thus, they can­not make their way through to the lym­phat­ic sys­tem, which is high­ly effi­cient at car­ry­ing lipopro­teins back to the blood­stream.
Pho­to by Ore­gon State Uni­ver­si­ty

Humans Are Starch Eaters

Here’s an inter­est­ing talk by Nathaniel Dominy, PhD, an Asso­ciate Pro­fes­sor of Anthro­pol­o­gy at Dart­mouth Uni­ver­si­ty. He explains the cen­tral role of diet in the amaz­ing world­wide suc­cess of the human species. If you can’t find enough to eat, you can’t do any of the oth­er things that you would need to do to help you and your chil­dren sur­vive.

He makes sev­er­al impor­tant points. One is that human beings are behav­ioral­ly “plas­tic.” He uses the term “plas­tic” in the sci­en­tif­ic sense, mean­ing that some­thing can take any shape. Our behav­ior is “plas­tic” because it can eas­i­ly be reshaped. As he point­ed out, human beings can adapt to many dif­fer­ent cli­mates because we have learned to make and wear clothes. We can also learn to eat lots of dif­fer­ent foods.

One type of food that is avail­able every­where except the Artic is starchy foods. All of the ener­gy in our diet comes from sun­light, which green plants use to make glu­cose out of car­bon diox­ide and water. Plants then store a lot of this glu­cose in the form of starch, often in their roots or tubers and in their seeds. Unfor­tu­nate­ly, starch is hard to digest. To digest it, we use amy­lase, an enzyme that con­verts the starch back to glu­cose.

Dominy sus­pects that our ances­tors’ abil­i­ty to rec­og­nize and use tuber-form­ing plants opened up a food source unknown to oth­er pri­mates. “It’s kind of a gold mine. All you have to do is dig it up.

Dominy points out that, when com­pared with oth­er pri­mates, human beings have extra copies of the gene for the starch-digest­ing enzyme amy­lase. As a result, we have a lot more amy­lase in our sali­va than goril­las or chim­panzees do. Peo­ple from soci­eties that depend heav­i­ly on starchy diets have sev­er­al more extra copies of the amy­lase gene and there­fore pro­duce a lot more amy­lase in their sali­va. In oth­er words, they have become genet­i­cal­ly more effi­cient at digest­ing starch­es. This kind of change can be seen in genet­i­cal­ly relat­ed pop­u­la­tions that have been adapt­ing to dif­fer­ent diets for only a few thou­sand years.

Although humans can and do eat prac­ti­cal­ly any­thing (we are behav­ioral­ly plas­tic), that doesn’t mean that we are well adapt­ed to a meat-based diet. As he puts it, “Anatom­i­cal­ly, we’re not adapt­ed to meat at all…. We sim­ply don’t have the adap­ta­tions that you would need to chew meat effi­cient­ly. Any­one can look at the teeth of their dog or cat and see what your teeth should look like if you’re going to eat meat. Our teeth don’t match.” Dominy con­cludes, “The fun­da­men­tal com­po­nent of the human diet is a mix of plant foods, with a large amount of starch com­ing from tubers and seeds.”

In this con­text, I’d point out that the adap­ta­tions to a meaty diet go far beyond the shape of the teeth. Even though dogs often eat a fat­ty, meaty diet, they gen­er­al­ly don’t get high cho­les­terol or ath­er­o­scle­ro­sis unless they also have a thy­roid dis­or­der that upsets their cho­les­terol metab­o­lism. In con­trast, human beings that eat a fat­ty, meaty diet are much more sus­cep­ti­ble than dogs are to high cho­les­terol and ath­er­o­scle­ro­sis. That explains why ath­er­o­scle­ro­sis is the lead­ing cause of death in the Unit­ed States but prac­ti­cal­ly nonex­is­tent in soci­eties where peo­ple eat a low-fat, plant-based diet.

How Low Should Your Cholesterol Levels Be?

Ide­al­ly, your total cho­les­terol should be below 150 mg/dL. Accord­ing to William Castel­li, who was the med­ical direc­tor of the Fram­ing­ham Heart Study for many years, peo­ple with a total cho­les­terol val­ue of less than 150 mg/dL sim­ply don’t get heart attacks. And once someone’s total cho­les­terol is that low, the ratio between the “good” and “bad” cho­les­terol sim­ply doesn’t mat­ter.

The total cho­les­terol val­ue is the sin­gle most impor­tant clue to a person’s risk of heart attack. Once the cho­les­terol lev­els in the blood rise to, say, the mid-160s, then the ratio of good ver­sus bad cho­les­terol (HDL ver­sus LDL) real­ly starts to mat­ter.

William Castel­li once explained, “Four out of five peo­ple on this earth can’t get their cho­les­terol over 150; they don’t get heart attacks. One out of five peo­ple can’t get their cho­les­terol down to 150. They do get heart attacks. And almost all of them live in afflu­ent coun­tries.” The “four out of five peo­ple” Castel­li meant live in soci­eties that eat a low-fat, high-fiber, large­ly plant-based diet. That kind of diet keeps blood cho­les­terol lev­els nat­u­ral­ly low.

He Should Have Won the Nobel Prize!

In 1913, a Russ­ian pathol­o­gist named Niko­lai Anitschkow fig­ured out the cause of ath­er­o­scle­ro­sis, which is the under­ly­ing cause of near­ly all heart attacks and most strokes. He even pub­lished his find­ings in the major inter­na­tion­al med­ical jour­nals of his day. He should have won the Nobel Prize. If peo­ple had rec­og­nized the impor­tance of his work, mil­lions of pre­ma­ture deaths could have been avoid­ed.

By the late 19th cen­tu­ry, pathol­o­gists knew that peo­ple who had died of heart attacks and strokes tend­ed to have a lot of softy, fat­ty mate­r­i­al stuck to the inner walls of their arter­ies. This mate­r­i­al even­tu­al­ly hard­ens with the buildup of scar tis­sue and cal­ci­um deposits. The pres­ence of this mate­r­i­al is called ath­er­o­scle­ro­sis, which means hard­en­ing of the arter­ies. The mate­r­i­al itself is called plaque.

In its ear­ly stages, ath­er­o­scle­rot­ic plaque looks and feels like cheese­cake. In 1910, a Ger­man chemist named Adolf Win­daus showed that like real cheese­cake, ath­er­o­scle­rot­ic plaque is rich in cho­les­terol. Because of his work on the chem­istry of sterols, Win­daus won the Nobel Prize in chem­istry in 1928.

As soon as Win­daus pub­lished his find­ings about the cho­les­terol in plaque, Niko­lai Anitschkow start­ed an impor­tant series of exper­i­ments at the Mil­i­tary Med­ical Acad­e­my in St. Peters­burg. Anitschkow dis­solved some puri­fied cho­les­terol in sun­flower oil and fed it to some rab­bits. Con­trol rab­bits got some sun­flower oil with­out added cho­les­terol. The rab­bits that got cho­les­terol in their sun­flower oil got ath­er­o­scle­rot­ic plaque, but the con­trol rab­bits did not. To the naked eye and under a micro­scope, the plaque from rab­bit arter­ies looked a lot like the plaque from human arter­ies.

Anitschkow and his cowork­ers dis­cov­ered a lot of impor­tant things about ath­er­o­scle­ro­sis in those ear­ly exper­i­ments. As cho­les­terol researcher Jon Gof­man argued,

If the full sig­nif­i­cance of his find­ings had been appre­ci­at­ed at the time, we might have saved more than 30 years in the long strug­gle to set­tle the ‘cho­les­terol con­tro­ver­sy’ and Anitschkow might have won a Nobel Prize. Instead, his find­ings were large­ly reject­ed or at least not fol­lowed up. Seri­ous research on the role of cho­les­terol in human ath­er­o­scle­ro­sis did not real­ly get under­way until the 1940s.

Why were Anitschkow’s find­ings ignored? Because they couldn’t be repeat­ed in dogs. As a result, many sci­en­tists assumed that the find­ings wouldn’t apply to human beings, either. That’s an idi­ot­ic assump­tion, because ath­er­o­scle­ro­sis is rare in dogs, which are nat­ur­al car­ni­vores. Anitschkow guessed cor­rect­ly that dogs and oth­er car­ni­vores are good at excret­ing excess cho­les­terol. Human beings and rab­bits are not. Trag­i­cal­ly, no one lis­tened, prob­a­bly because they’d rather eat meat than rab­bit food.

My Cholesterol Is Too Low for the Heart Attack Risk Calculator!

I tried to use the Nation­al Cho­les­terol Edu­ca­tion Program’s Risk Assess­ment Tool for Esti­mat­ing Your 10-Year Risk of Hav­ing a Heart Attack. I entered my data on the form, and I got back an error mes­sage, telling me to enter a total cho­les­terol val­ue of 130 or greater! Accord­ing to the cal­cu­la­tor, even if my cho­les­terol went up to 130 mg/dL, I’d still have less than a 1% chance of hav­ing a heart attack with­in the next 10 years.

(Note: here’s a live ver­sion of the tool, which does not give an error mes­sage: https://www.cardiosmart.org/healthwise/calc/006/calc006)

If I ran the Nation­al Cho­les­terol Edu­ca­tion Pro­gram, I’d real­ly edu­cate peo­ple about cho­les­terol. I’d tell them the sim­ple truth: that when you keep your total cho­les­terol at less than 150 mg/dL, coro­nary artery dis­ease ceas­es to exist. Near­ly every­one can eas­i­ly achieve that goal by eat­ing a low-fat (<10% of calo­ries), plant-based diet.

Instead, the NCEP tells peo­ple that a total cho­les­terol lev­el of  up to 200 mg/dL is “desir­able.” Lots of peo­ple with this “desir­able” cho­les­terol lev­el are dying of heart attacks, which is why many peo­ple, includ­ing many doc­tors, are con­fused.Pho­to by win­nifredx­oxo

Weight and Cholesterol: When Average Is Abnormal

I just dis­cov­ered that I’m nor­mal, which means that I’m way below aver­age. I’m 5 foot 5 inch­es tall and weigh about 125 pounds. That gives me a body mass index of 20.8, which is nor­mal. Yet it also means that I’m skin­nier than about 95% of the Amer­i­can women my age. To become offi­cial­ly over­weight, I’d have to gain at least 25 pounds. To be as fat as the aver­age Amer­i­can, I’d have to gain a total of 40 pounds. To qual­i­fy as obese, I’d have to gain a total of 50 pounds.

If you live in the Unit­ed States, you have prob­a­bly noticed that most of the peo­ple around you weigh more than they should. That’s because you prob­a­bly know, more or less instinc­tive­ly, what healthy peo­ple are sup­posed to look like. Unfor­tu­nate­ly, we can’t auto­mat­i­cal­ly rec­og­nize that some of our oth­er mea­sure­ments, such as our total cho­les­terol val­ues, are also wild­ly abnor­mal. That’s because nobody has an instinc­tive feel for what healthy blood val­ues are sup­posed to be. It’s tempt­ing to eval­u­ate them by com­par­ing them to the aver­age val­ues for our pop­u­la­tion, but how can we tell if the aver­age val­ue in our pop­u­la­tion is nor­mal or abnor­mal?

The U.S. fed­er­al government’s “Healthy Peo­ple 2010” guide­lines regard­ed total cho­les­terol of 240 mg/dL as “high” and a lev­el of 200 mg/dL as “desir­able.” Yet peo­ple are still at risk for heart dis­ease as long as their total cho­les­terol is above 150 mg/dL. The last time my blood was test­ed, my total cho­les­terol was 120 mg/dL. Accord­ing to sta­tis­tics from the Cen­ters from Dis­eases Con­trol and Pre­ven­tion, my total cho­les­terol lev­el is unusu­al­ly low. More than 95% of the Amer­i­cans in my age-group have a total cho­les­terol val­ue that’s way high­er than mine. Yet I sus­pect that my cho­les­terol lev­els, like my weight, are nor­mal and healthy. It’s the aver­age per­son who’s dan­ger­ous­ly abnor­mal.

The num­bers are stag­ger­ing. Peo­ple whose cho­les­terol lev­el is “high” by Amer­i­can stan­dards (over 240 mg/dL) have more than twice as much cho­les­terol in their blood as I have. The aver­age Amer­i­can has a total cho­les­terol lev­el of about 200 mg/dL. This means that even the aver­age per­son has far more cho­les­terol in his or her blood than I do. No won­der their arter­ies are get­ting clogged!

My blood cho­les­terol lev­el may seem amaz­ing­ly low, but it’s about aver­age for some­one in rur­al Chi­na. In the late 1990s, the Chi­na-Cor­nell-Oxford Project found that the aver­age total cho­les­terol lev­el in rur­al Chi­nese peo­ple was 127 mg/dL. As a result, heart attacks were rare in Chi­na. Over­all, Amer­i­can men were 17 times as like­ly as Chi­nese men to get a heart attack. Amer­i­can women were about 6 times as like­ly as Chi­nese women to get heart attacks.

In some areas of rur­al Chi­na, coro­nary artery dis­ease was prac­ti­cal­ly nonex­is­tent. A pop­u­la­tion of a few hun­dred thou­sand peo­ple could go for a cou­ple of years with­out any­one under age 65 dying of a coro­nary. Not one per­son. The study didn’t ana­lyze the caus­es of death among the elder­ly, but there prob­a­bly weren’t many coro­nar­ies among peo­ple over 65, either.

Why were cho­les­terol val­ues and rates of coro­nary artery dis­ease so low in Chi­na? The study showed that diet makes the dif­fer­ence. Over­all, the Chi­nese were eat­ing only about a tenth as much ani­mal pro­tein and three times as much fiber as Amer­i­cans were eat­ing. The less ani­mal pro­tein peo­ple ate, the low­er their cho­les­terol val­ues were, and the less like­ly they were to die of heart dis­ease and var­i­ous can­cers. There didn’t seem to be any “safe” lev­el of intake of ani­mal pro­tein. Eat­ing even a small amount of ani­mal pro­tein pro­duced a small but mea­sur­able increase in risk. On the oth­er hand, the more veg­eta­bles peo­ple ate, the safer they were.

My cho­les­terol val­ues look like those of some­one from rur­al Chi­na because I eat no ani­mal pro­tein but lots of rice and oth­er grains and veg­eta­bles and beans and fruit. Any­one who thinks that this kind of diet is bor­ing or unsat­is­fy­ing has sim­ply nev­er had din­ner at my house.

I know from read­ing the sci­en­tif­ic lit­er­a­ture on nutri­tion that peo­ple in the Unit­ed States could dra­mat­i­cal­ly improve their health and increase their life expectan­cy by shift­ing from the stan­dard Amer­i­can diet, with its heavy empha­sis on ani­mal pro­tein and its heavy load of fat, to a diet based on unre­fined plant foods. This sim­ple cor­rec­tion in the diet would enable peo­ple to drop to a nor­mal weight with­out count­ing calo­ries or lim­it­ing their por­tions. It would prac­ti­cal­ly elim­i­nate heart dis­ease and great­ly reduce the risk of oth­er dis­eases. So why doesn’t our gov­ern­ment tell us about this?

Worse yet, our gov­ern­ment is still urg­ing peo­ple to eat ani­mal pro­tein. Although the Healthy Peo­ple 2020 goals sup­pos­ed­ly “reflect strong sci­ence,” their dietary advice flies in the face of what we learned from the Chi­na-Cor­nell-Oxford study. In par­tic­u­lar, the healthypeople.gov Web site says the fol­low­ing: “Amer­i­cans with a health­ful diet con­sume a vari­ety of nutri­ent-dense foods with­in and across the food groups, espe­cial­ly whole grains, fruits, veg­eta­bles, low-fat or fat-free milk or milk prod­ucts, and lean meats and oth­er pro­tein sources.” Since we know from the Chi­na-Cor­nell-Oxford study that eat­ing ani­mal pro­tein is the major con­tribut­ing cause of our major cause of death, and that there’s no safe lev­el of intake of such foods, why in the name of good com­mon sense is our gov­ern­ment say­ing that a diet that includes these foods is health­ful?

What’s Next, an Atherosclerosis Acceptance Movement?

The Hidden Danger of the “Fat Acceptance” Movement

You know the old say­ing, “If some­thing is too good to be true….” Well, the “fat accep­tance” move­ment is telling peo­ple some­thing that sounds too good to be true. They are insist­ing that peo­ple can be “healthy at any size” and some­times even that being over­weight is health­i­er than being slim. They’re wrong, and the smarter and more edu­cat­ed peo­ple among the “fat accep­tance” move­ment should know bet­ter. They “cher­ry pick” mis­lead­ing find­ings from a few stud­ies and ignore a vast sci­en­tif­ic lit­er­a­ture on the effects of diet on health. Such behav­ior is sick­en­ing, and the advice they give is dan­ger­ous.

Here’s the sim­ple truth: excess body fat is only one of the pos­si­ble bad effects of eat­ing the wrong kind of food. Eat­ing too much fat and too much ani­mal pro­tein can send you to an ear­ly grave even if you are thin and exer­cise a lot. The clas­sic exam­ple is Jim Fixx, author of The Com­plete Book of Run­ning, a 1977 best­seller that launched the run­ning boom. Fixx had claimed that his gru­el­ing exer­cise reg­i­men, which had enabled him to lose 60 pounds, allowed him to eat as much as he want­ed of what­ev­er he want­ed. When I read that in his book, I thought, “But what about cho­les­terol?” So I was sad­dened, but not sur­prised, when Fixx dropped dead at age 52 of a heart attack while run­ning. To my dis­gust, the media react­ed to his death by ask­ing whether run­ning was good or bad for you, ignor­ing the obvi­ous dietary angle to the sto­ry.

The sim­ple truth is that eat­ing the wrong kind of food can kill you, even if it doesn’t make you fat. Anoth­er sim­ple truth is that you can’t out­run cho­les­terol. As a mem­ber of the high-IQ club Men­sa, Fixx should have been smart enough to fig­ure that out before it was too late. Unfor­tu­nate­ly, he believed what he want­ed to believe, and ate what­ev­er he want­ed to eat, and in the end it killed him.

As I men­tioned, obe­si­ty is only one of the bad effects that is like­ly to result from eat­ing the stan­dard Amer­i­can diet–not just the heav­i­ly processed “junk food” that every­one knows is bad for you, but the meat and dairy prod­ucts and eggs and fish that the US Depart­ment of Agri­cul­ture has been encour­ag­ing us to eat.

Col­lec­tive­ly, the bad effects of eat­ing the stan­dard Amer­i­can diet are called “West­ern dis­eases.” This is because med­ical doc­tors who had been trained in Europe and the Unit­ed States were stunned to find that these health prob­lems, which were com­mon back home, were rare to nonex­is­tent in Asia and Africa. Besides over­weight and obe­si­ty, they include heart dis­ease, dia­betes, var­i­ous can­cers, arthri­tis, vari­cose veins, mul­ti­ple scle­ro­sis, etc. etc. etc. West­ern dis­eases were (and still are) the major caus­es of death and dis­abil­i­ty in the Unit­ed States and Europe because peo­ple there eat too much ani­mal pro­tein and too much fat. These dis­eases were rare in Asia and Africa because the pop­u­la­tions were eat­ing a low-fat, large­ly plant-based diet. A mon­u­men­tal study of nutri­tion­al epi­demi­ol­o­gy in Chi­na (http://www.thechinastudy.com/) showed in detail how close­ly the con­sump­tion of ani­mal pro­tein and fat were linked to many of these dis­eases. The less ani­mal-based food and fat peo­ple ate, the health­i­er they could be.

The good news is that if you eat the diet that will pro­tect you against the oth­er “West­ern dis­eases,” your weight prob­lem will solve itself. Peo­ple who eat a low-fat (<10% of calo­ries) diet based on unre­fined plant foods rapid­ly become heart-attack-proof (total cho­les­terol, <150 mg/dL) and can pre­vent and even reverse many of the oth­er West­ern dis­eases. It’s hard to stay fat when you are eat­ing a tru­ly healthy diet. When over­weight Amer­i­cans switch to a low-fat, pure­ly plant-based diet, they lose weight eas­i­ly with­out hav­ing to count calo­ries or lim­it their por­tions. They can eat to their hearts’ con­tent and still stay slim. The “fat accep­tance” advo­cates over­look that obvi­ous fact.

The “fat accep­tance” advo­cates are right that thin does not equal healthy. But they are wrong when they say that you can be healthy at any size. Rather than wast­ing their time try­ing to make peo­ple feel bet­ter about being fat, they should work toward edu­cat­ing peo­ple about a tru­ly healthy diet, which will enable peo­ple to improve their own health and main­tain a desir­able weight with­out feel­ing hun­gry. The activists should also use their polit­i­cal clout to improve the nutri­tion cur­ricu­lum at med­ical schools, which has been shown repeat­ed­ly over the past 40 years to be inad­e­quate.

On one point, I do agree with the fat accep­tance advo­cates. I think that peo­ple should be treat­ed with respect regard­less of their size and state of health. How­ev­er, I feel that over­weight peo­ple deserve to be told the truth about how their weight affects their health and about how their food choic­es affect both their health and their weight.

How Low Should Total Cholesterol Be?

Below 150 mg/dL, Accord­ing to Dr. Cald­well Essel­styn

Based on the ground­break­ing results of his 20-year nutri­tion­al study—the longest study of its kind ever conducted—this book explains, with irrefutable sci­en­tif­ic evi­dence, how we can end the heart dis­ease epi­dem­ic in this coun­try for­ev­er by chang­ing what we eat. Here, Dr. Essel­styn con­vinc­ing­ly argues that a plant-based, oil-free diet can not only pre­vent and stop the pro­gres­sion of heart dis­ease, but also reverse its effects.” http://www.heartattackproof.com/

Heart attack is vir­tu­al­ly nonex­is­tent in pop­u­la­tions whose heav­i­ly plant-based diet keeps the aver­age person’s total cho­les­terol below 150 mg/dL.

Going Ape Lowers Cholesterol

A Goril­la-Style Diet Was Com­pa­ra­ble to Lovas­tatin in Low­er­ing Cho­les­terol

Maybe the ben­e­fits of the “Mediter­ranean diet” come from the rata­touille, not from the olive oil and fish:

http://www.newscientist.com/article/dn3966

In case you are won­der­ing, aubergine means egg­plant.