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/)