We’re Making the Gorillas Sick! Stay Away From Them!

When I was a child, I saw that the goril­las, unlike all the oth­er ani­mals at the Colum­bus Zoo, were behind glass. My par­ents said that this was to keep the goril­las from catch­ing dis­eases like tuber­cu­lo­sis from the peo­ple who came to see them.

Goril­las look almost human because their genes are strik­ing­ly sim­i­lar to ours. Chim­panzees and bono­bos look even more human-like because their genes are even more like ours. The more DNA you have in com­mon, the more like­ly it is that you’ll be sus­cep­ti­ble to the same bac­te­ria and virus­es. Human beings prob­a­bly caught the first cas­es of AIDS from chim­panzees. Now there is a report from the U.S. Cen­ters for Dis­ease Con­trol and Pre­ven­tion that endan­gered wild goril­las are catch­ing a dead­ly virus from human beings! They are prob­a­bly catch­ing the dis­ease from the eco­tourists who go to see them!

On one hand, eco­tourism seems to be nec­es­sary to help pro­tect the goril­la habi­tat. On the oth­er hand, the dis­eases that the eco­tourists bring with them could be dead­ly to the goril­las.

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.

Calcium Supplements: More Heart Attacks, but Also More Osteoporosis

Women in the Unit­ed States are con­tin­u­al­ly pres­sured by their doc­tors and by the media to eat a high-cal­ci­um diet and take cal­ci­um sup­ple­ments, sup­pos­ed­ly to pre­vent osteo­poro­sis. I resist this advice, because I’ve known for more than 20 years that osteo­poro­sis is actu­al­ly most com­mon in the pop­u­la­tions with the high­est cal­ci­um intakes. Now, a study just pub­lished in the British Med­ical Jour­nal warns that cal­ci­um sup­ple­ments could also raise the risk of heart attack, which is the major cause of death in women in the Unit­ed States.

I found out about the link between high cal­ci­um intakes and osteo­poro­sis in the late 1980s, while I was edit­ing a hand­book for dieti­tians. The author wrote that osteo­poro­sis is com­mon only in soci­eties where peo­ple eat a lot of dairy prod­ucts. I was shocked by this infor­ma­tion. Lat­er on, I found that both the high pro­tein con­tent and the high cal­ci­um con­tent of dairy foods are impli­cat­ed in caus­ing osteo­poro­sis. For years, Har­vard pro­fes­sor Mark Heg­st­ed warned peo­ple that osteo­poro­sis was a result of the same kind of diet that caus­es heart dis­ease. He specif­i­cal­ly warned that high cal­ci­um intakes prob­a­bly make osteo­poro­sis worse. Sad­ly, his warn­ings fell on deaf ears.

Read­ing the arti­cle in the British Med­ical Jour­nal made me angry. The study it described was a meta-analy­sis, which means that it com­piled the results of sev­er­al clin­i­cal tri­als. The researchers found 15 clin­i­cal tri­als in which women were giv­en either cal­ci­um or place­bo, most­ly for the pre­ven­tion or treat­ment of osteo­poro­sis. What angered me was the dates of the stud­ies. The ear­li­est one was pub­lished in 1989, the lat­est in 2008. Even by the time the ear­li­est of those stud­ies was done, there was already plen­ty of rea­son to believe that cal­ci­um sup­ple­ments would have made the women’s osteo­poro­sis worse, not bet­ter. In oth­er words, human research sub­jects were sub­ject­ed to unnec­es­sary harm. That sort of thing is a huge vio­la­tion of med­ical research ethics. It’s also ille­gal in civ­i­lized coun­tries.

Med­ical researchers are sup­posed to do their home­work before they start enrolling human beings in a clin­i­cal tri­al. By the time that first study was done, it was already obvi­ous that high cal­ci­um intakes make osteo­poro­sis worse, not bet­ter. Har­vard pro­fes­sor Mark Heg­st­ed explained the prob­lem in an arti­cle pub­lished in 1986, before the first of the stud­ies includ­ed in the meta-analy­sis.

It’s bad enough that the aver­age doc­tor has had lit­tle to no train­ing in nutri­tion or dietet­ics. What’s even worse is that some of the doc­tors who are doing nutri­tion stud­ies evi­dent­ly don’t both­er to read the sci­en­tif­ic lit­er­a­ture on nutri­tion before they start exper­i­ment­ing on human beings.

Accord­ing to the arti­cle in the British Med­ical Jour­nal, there were 143 myocar­dial infarc­tions in the patients assigned to take cal­ci­um and 111 myocar­dial infarc­tions in the patients assigned to take a place­bo. If these women had been giv­en prop­er coun­sel­ing on how to make them­selves heart-attack-proof, all of these heart attacks could have been avoid­ed.

Pho­to by Ger­man Teno­rio

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

Accidentally Kosher for Passover!

Back when I was in high school, a friend of mine from an obser­vant Jew­ish fam­i­ly told me that her fam­i­ly often ate in veg­e­tar­i­an restau­rants. She explained that most of the Jew­ish dietary laws relat­ed to meat. If you ate in a restau­rant that nev­er served any meat prod­ucts, you would auto­mat­i­cal­ly be observ­ing most of the rules.

The excep­tion, of course, is Passover. Dur­ing Passover, Jews aren’t sup­posed to eat yeast-raised bread. This rule doesn’t just apply to wheat. It applies to four oth­er grains as well: bar­ley, rye, spelt, and oats. If any of these grains is allowed to sit in water for longer than 18 min­utes, it becomes chometz. It’s against Jew­ish dietary law to eat, own, or ben­e­fit from chometz at any time dur­ing Passover.

Of course, peo­ple with celi­ac dis­ease can’t eat wheat, bar­ley, rye, or spelt—even if they haven’t become chometz—at any time of year. In oth­er words, prod­ucts that are gluten-free and don’t con­tain oats are auto­mat­i­cal­ly nev­er chometz.

Ashke­nazi Jews are also sup­posed to refrain from eat­ing kit­niy­ot dur­ing Passover. Kit­niy­ot con­sists of grains and puls­es (such as corn, rice, beans, lentils, peas, and pos­si­bly peanuts) that could be con­fused with chometz. Still, a gluten-free veg­an cook­book would be a good place to look for good recipes to use dur­ing Passover. Lots of those recipes are acci­den­tal­ly Kosher for Passover!

Pho­to by Cen­ter for Jew­ish His­to­ry, NYC

The Dutch Hunger Winter

The best data that we have on the effects of star­va­tion dur­ing preg­nan­cy came about as the result of a war crime. In retal­i­a­tion for a rail­road strike that under­mined the Ger­man military’s abil­i­ty to resist the advanc­ing Allied forces, the Ger­mans cut off food sup­plies to the still-occu­pied west­ern part of the Nether­lands in Octo­ber of 1944. Thus began a famine that last­ed until May of 1945. This appalling, crim­i­nal star­va­tion of a civil­ian pop­u­la­tion caused near­ly 20,000 excess deaths, main­ly in elder­ly men. It also had ter­ri­ble effects on the sur­vivors, includ­ing preg­nant women and their babies. The effects of the Dutch Hunger Win­ter on sur­vivors are still being stud­ied today.

From a sci­en­tif­ic stand­point, the data from the Dutch Hunger Win­ter are par­tic­u­lar­ly valu­able. Here was a pop­u­la­tion that went from being well-fed to being bad­ly starved and then went back to being well-fed. The pre­cise dates of the food depri­va­tion were known and could be cor­re­lat­ed with birth records. After the war, sci­en­tists stud­ied fam­i­lies that had been exposed to the famine. They paid par­tic­u­lar atten­tion to peo­ple who had been in their mother’s womb dur­ing the famine.

The main thing that we’ve learned from the Dutch Hunger Win­ter is that star­va­tion is bad, espe­cial­ly for preg­nant women. The next time you hear of some­one advo­cat­ing some pol­i­cy that would end up starv­ing a civil­ian pop­u­la­tion, do what­ev­er you can to pre­vent or stop it.

The oth­er valu­able les­son learned from the Dutch Hunger Win­ter was the cause of celi­ac dis­ease. When wheat became scarce and peo­ple had to sub­sist on oth­er foods, such as tulip bulbs, chil­dren with celi­ac dis­ease improved dra­mat­i­cal­ly. Cur­rent­ly, a diet that is free of wheat, rye, and bar­ley is the stan­dard way to man­age celi­ac dis­ease.

Movie star Audrey Hep­burn, who sur­vived the Dutch Hunger Win­ter, served as Good­will Ambas­sador for the Unit­ed Nations Children’s Fund (UNICEF) from 1988 to the end of her life.

Pho­to by Eliza­Pey­ton

If It’s Becoming More Common, It’s Not Genetic!

Don’t get me wrong. I think that the Human Genome Project was a great idea. How­ev­er, I don’t think that genet­ic stud­ies are going to help us unrav­el our main caus­es of death and dis­abil­i­ty in the Unit­ed States. That’s because they are large­ly the result of our food, not our genes. You can tell this from the sim­ple fact that the rates of these dis­eases go up and down, depend­ing on how a pop­u­la­tion eats.

The rate of tru­ly genet­ic dis­eases (such as hemo­phil­ia or cys­tic fibro­sis) stays remark­ably sta­ble in a pop­u­la­tion from one gen­er­a­tion to the next. The only way it could increase is if there were a sud­den wave of immi­gra­tion of peo­ple car­ry­ing the gene (in which case, the dis­ease would most­ly be in the immi­grants and their chil­dren) or if the peo­ple with the gene sud­den­ly became much more fer­tile (which is unlike­ly).

When you see the rate of a dis­ease go up and down dra­mat­i­cal­ly with­in the space of 10 years, you know for sure that the cause of that change is envi­ron­men­tal, not genet­ic. The clas­sic illus­tra­tion is the sharp decline in heart dis­ease in Nor­way dur­ing World War II. After the Nazis invad­ed Nor­way (and stole a lot of their farm ani­mals), the Nor­we­gian pop­u­la­tion had to shift to a low-fat, plant-based diet. As a result, the dis­eases of afflu­ence (heart dis­ease, type 2 dia­betes, mul­ti­ple scle­ro­sis) became much less com­mon. The rates of those dis­eases went right back up again after the war end­ed and peo­ple went back to their old ways of eat­ing.

Anoth­er clue to whether a dis­ease is genet­ic or envi­ron­men­tal comes from its geo­graph­ic dis­tri­b­u­tion. If a dis­ease is most com­mon in an area with small gene pool, it’s like­ly to be genet­ic. Exam­ples include the hered­i­tary deaf­ness that was once com­mon on Martha’s Vine­yard and Tay-Sachs dis­ease in East­ern Euro­pean Jews and French Cana­di­ans. These are reces­sive gene dis­eases. You can get the dis­ease only if you got the same defec­tive gene from both par­ents, which is most like­ly to hap­pen if they are relat­ed to each oth­er.

On the oth­er hand, if a dis­ease is most com­mon in an area whose pop­u­la­tion came from a wide vari­ety of immi­grants, then you can bet your bot­tom dol­lar that the under­ly­ing cause for the high rate of the dis­ease is envi­ron­men­tal, not genet­ic. The clas­sic exam­ple of this is Parkin­son dis­ease, which is most com­mon in Buenos Aires, Argenti­na. Although there may be some genes that pre­dis­pose a per­son to Parkin­son dis­ease, espe­cial­ly the ear­ly-onset form, the fact that the world’s high­est rate is in a pop­u­la­tion made up of recent immi­gra­tion from many dif­fer­ent places tells me that the major risk fac­tor is some­thing in the envi­ron­ment. Con­sid­er­ing that the peo­ple of Buenos Aires also eat more beef than any­one else in the world, I’d be will­ing to bet that the envi­ron­men­tal fac­tor is red meat con­sump­tion.

Pho­to by Inter­net Archive Book Images

The Imaginary Historical Decrease in Fat Consumption

Late­ly, I’ve seen many “experts” on nutri­tion claim that low-fat foods make peo­ple fat. As part of the “evi­dence” to back up this non­sense, they claim that the recent increase in pop­u­lar­i­ty of low-fat foods is an under­ly­ing cause of our obe­si­ty epi­dem­ic. They must think that I’m too lazy or stu­pid to look up the real data for myself.

I entered the term “fat con­sump­tion trends” into Google, and with­in a sec­ond or two I found this arti­cle: Trends in Intake of Ener­gy and Macronu­tri­ents — Unit­ed States, 1971–2000. This arti­cle reports the trends that the CDC found when they ana­lyzed data from four Nation­al Health and Nutri­tion Exam­i­na­tion Sur­veys (NHANES), the first of which was con­duct­ed in 1971–1974 and the last of which was con­duct­ed in 1999–2000. These sur­veys revealed that men and women were eat­ing more calo­ries and more fat in 1999–2000 than they had been eat­ing in the ear­ly 1970s. How­ev­er, they were also eat­ing so much more sug­ar that the per­cent­age of their calo­ries that came from fat went down slight­ly.

In oth­er words, peo­ple are get­ting fat­ter because they are eat­ing more calo­ries, includ­ing more fat. In con­trast, Japan­ese chil­dren have been get­ting fat­ter and run­ning a risk of type 2 dia­betes even though they have been eat­ing few­er calo­ries. It’s because of a shift from their tra­di­tion­al starchy diet to a more West­ern­ized, high­er-fat diet.

As I’ve explained in detail here, it’s easy to fat­ten on fat but much hard­er to fat­ten on starch­es.

Why Gorillas, Why Not Chimpanzees?

Many peo­ple have asked me, why do you ask where goril­las get their pro­tein, when our bod­ies and our body chem­istry more close­ly resem­ble those of chim­panzees? My answer is that goril­las are much big­ger and more pow­er­ful than chim­panzees. Last night, I saw a muse­um exhib­it that com­pared a goril­la skull to a chim­panzee skull and a human skull. (They might have been mod­els. It was hard to tell.) The goril­la skull was huge! The chim­panzee skull was about the same size as a human skull.

The oth­er rea­son is that goril­las eat a much more strict­ly plant-based diet. Chim­panzees hunt once in a while, and they often eat their kill. Even so, they still eat a lot less meat than just about any human pop­u­la­tion. Nev­er­the­less, I was afraid that the fact they eat a lit­tle bit of meat now and then would mud­dy the waters.

My point is this. Most of the real­ly big and pow­er­ful land ani­mals got big and pow­er­ful by eat­ing plants. They don’t wor­ry about get­ting a pro­tein defi­cien­cy on a plant-based diet, and nei­ther should you.


(Image cour­tesy of Mahla­ti­ni Lux­u­ry Safari, https://www.mahlatini.com/gorilla-trekking-safaris/)