“When ranked in order of importance, among the interventions available to prevent stroke, the three most important are probably diet, smoking cessation, and blood pressure control.” Most of us these days are doing pretty good about not smoking, but less than half of us exercise enough. And, according to the American Heart Association, only 1 in 1,000 Americans is eating a healthy diet and less than 1 in 10 is even eating a moderately healthy diet, as you can see in the graph below and at 0:41 in my video Do Vegetarians Really Have Higher Stroke Risk?. Why does it matter? It matters because “diet is an important part of stroke prevention. Reducing sodium intake, avoiding egg yolks, limiting the intake of animal flesh (particularly red meat), and increasing the intake of whole grains, fruits, vegetables, and lentils….Like the sugar industry, the meat and egg industries spend hundreds of millions of dollars on propaganda, unfortunately with great success.” 

The paper goes on to say, “Box 1 provides links to information about the issue.” I was excited to click on the hyperlink for “Box 1” and was so honored to see four links to my videos on egg industry propaganda, as you can see below and at 1:08 in my video. 

The strongest evidence for stroke protection lies in increasing fruit and vegetable intake, with more uncertainty regarding “the role of whole grains, animal products, and dietary patterns,” such as vegetarian diets. One would expect meat-free diets would do great. Meta-analyses have found that vegetarian diets lower cholesterol and blood pressure, as well as enhance weight loss and blood sugar control, and vegan diets may work even better. All the key biomarkers are going in the right direction. Given this, you may be surprised to learn that there hadn’t been any studies on the incidence of stroke in vegetarians and vegans until now. And if you think that is surprising, wait until you hear the results. 

“Risks of Ischaemic Heart Disease and Stroke in Meat Eaters, Fish Eaters, and Vegetarians Over 18 Years of Follow-Up: Results from the Prospective EPIC-Oxford Study”: There was less heart disease among vegetarians (by which the researchers meant vegetarians and vegans combined). No surprise. Been there, done that. But there was more stroke, as you can see below, and at 2:14 in my video. 

An understandable knee-jerk reaction might be: Wait a second, who did this study? Was there a conflict of interest? This is EPIC-Oxford, world-class researchers whose conflicts of interest may be more likely to read: “I am a member of the Vegan Society.”

What about overadjustment? When the numbers over ten years were crunched, the researchers found 15 strokes for every 1,000 meat eaters, compared to only 9 strokes for every 1,000 vegetarians and vegans, as you can see below and at 2:41 in my video. In that case, how can they say there were more strokes in the vegetarians? This was after adjusting for a variety of factors. The vegetarians were less likely to smoke, for example, so you’d want to cancel that out by adjusting for smoking to effectively compare the stroke risk of nonsmoking vegetarians to nonsmoking meat eaters. If you want to know how a vegetarian diet itself affects stroke rates, you want to cancel out these non-diet-related factors. Sometimes, though, you can overadjust. 

The sugar industry does this all the time. This is how it works: Imagine you just got a grant from the soda industry to study the effect of soda on the childhood obesity epidemic. What could you possibly do after putting all the studies together to conclude that there was a “near zero” effect of sugary beverage consumption on body weight? Well, since you know that drinking liquid candy can lead to excess calories that can lead to obesity, if you control for calories, if you control for a factor that’s in the causal chain, effectively only comparing soda drinkers who take in the same number of calories as non-soda-drinkers, then you could undermine the soda-to-obesity effect, and that’s exactly what they did. That introduces “over adjustment bias.” Instead of just controlling for some unrelated factor, you control for an intermediate variable on the cause-and-effect pathway between exposure and outcome.

Overadjustment is how meat and dairy industry-funded researchers have been accused of “obscuring true associations” between saturated fat and cardiovascular disease. We know that saturated fat increases cholesterol, which increases heart disease risk. Therefore, if you control for cholesterol, effectively only comparing saturated fat eaters with the same cholesterol levels as non-saturated-fat eaters, that could undermine the saturated fat-to-heart disease effect.

Let’s get back to the EPIC-Oxford study. Since vegetarian eating lowers blood pressure and a lowered blood pressure leads to less stroke, controlling for blood pressure would be an overadjustment, effectively only comparing vegetarians to meat eaters with the same low blood pressure. That’s not fair, since lower blood pressure is one of the benefits of vegetarian eating, not some unrelated factor like smoking. So, that would undermine the afforded protection. Did the researchers do that? No. They only adjusted for unrelated factors, like education, socioeconomic class, smoking, exercise, and alcohol. That’s what you want. You want to tease out the effects of a vegetarian diet on stroke risk. You want to try to equalize everything else to tease out the effects of just the dietary choice. And, since the meat eaters in the study were an average of ten years older than the vegetarians, you can see how vegetarians could come out worse after adjusting for that. Since stroke risk can increase exponentially with age, you can see how 9 strokes among 1,000 vegetarians in their 40s could be worse than 15 strokes among 1,000 meat-eaters in their 50s. 

The fact that vegetarians had greater stroke risk despite their lower blood pressure suggests there’s something about meat-free diets that so increases stroke risk it’s enough to cancel out the blood pressure benefits. But, even if that’s true, you would still want to eat that way. As you can see in the graph below and at 6:16 in my video, stroke is our fifth leading cause of death, whereas heart disease is number one. 

So, yes, in the study, there were more cases of stroke in vegetarians, but there were fewer cases of heart disease, as you can see below and at 6:29. If there is something increasing stroke risk in vegetarians, it would be nice to know what it is in hopes of figuring out how to get the best of both worlds. This is the question we will turn to next. 

I called it 21 years ago. There’s an old video of me on YouTube where I air my concerns about stroke risk in vegetarians and vegans. (You can tell it’s from 2003 by my cutting-edge use of advanced whiteboard technology and the fact that I still had hair.) The good news is that I think there’s an easy fix.

This is the third in a 12-video series on stroke risk. Links to the others are in the related posts below.

Lipoprotein A, also known as Lp(a), is an independent, genetic, and causal factor for cardiovascular disease and heart attacks. At any level of LDL cholesterol, our risk of heart attack and stroke is two- to three-fold higher when our Lp(a) is elevated. With a high enough Lp(a) level, atherosclerosis continues to progress even if we get our LDL cholesterol way down, which may help explain why so many people continue to have heart attacks and strokes even under treatment for high cholesterol. It’s been suggested that “it would be worthwhile to check Lp(a) levels in a patient who has suffered an event but has no traditional risk factors to explain it.” What’s the point of checking it, though, if there isn’t much we can do about it? “To date, no drug to reduce circulating Lp(a) levels has been approved for clinical use.”

Some researchers blame our lack of knowledge on the fact that Lp(a) is not found in typical lab animals, like rats and mice. It’s only found in two places in nature: primates and hedgehogs. Hedgehogs? How strange is that? No wonder Lp(a) is “an enigmatic protein that has mystified medical scientists ever since” it was first discovered more than half a century ago. But who needs mice when you have men? The level in our bloodstream is “primarily determined” by genetics. For the longest time, Lp(a) was not thought to be significantly influenced by factors such as diet. Given its similarity to LDL, though, one might assume lifestyle changes, “such as increased physical activity or the adoption of a healthy diet,” would help. “However, the effects of these interventions on Lp(a) concentrations are so far either only marginal or lacking in evidence,” but might that be because they have not tried a plant-based diet yet?

As I discuss in my video How to Lower Lp(a) with Diet, when it comes to raising LDL cholesterol, we’ve known for years that the trans fats found in meat and dairy are just as bad as the industrially produced trans fats found in partially hydrogenated oil and junk food. But, when it comes to Lp(a), as you can see below and at 2:05 in my video, trans fats from meat and dairy appear to be even worse. 

Just cutting out meat and following a lacto-ovo vegetarian diet did not appear to help, but, as you can see below and at 2:19 in my video, when study participants were put on a whole food, plant-based diet packed with a dozen servings of fruits and vegetables a day, their Lp(a) levels dropped by 16 percent within four weeks. 

Of course, in those 30 days, the study subjects also lost about 15 pounds, as you can see below and at 2:28, but weight loss does not appear to affect Lp(a) levels, so you figure that it must have been due to the diet. 

If you’re already eating a healthy plant-based diet and your Lp(a) levels are still too high, are there any particular foods that can help? As with cholesterol, even if the average total cholesterol of those eating strictly plant-based may be right on target at less than 150, with an LDL under 70, there’s a bell curve with plus or minus 30 points that fall on either side, as you can see below and at 2:45 in my video. 

Enter the “Portfolio Diet,” which is not only plant-based, but also adds specific cholesterol-lowing foods—so, think nuts, beans, oatmeal, and berries to drag cholesterol down even further. The infographic is below and at 3:11 in my video.  

What about Lp(a)? Nuts have been put to the test. Two and a half ounces of almonds every day dropped levels, but only by about 8 percent. That is better than another nut study, though, that found no effect at all, as you can see below and at 3:29 in my video. An additional study found “no significant changes,” and researchers reported that subjects in their study “did not experience a change in Lp(a).” Ah, nuts.  

There is one plant that appears to drop Lp(a) levels by 20 percent, which is enough to take people exceeding the U.S. cut-off down to a more optimum level. And that plant is a fruit: Emblica officinalis, otherwise known as amla or Indian gooseberry. A randomized, double-blind, placebo-controlled study asked smokers before and after the trial about their “mouth hygiene, cough with expectoration, shortness of breath on exertion, loss of appetite, feelings of impending doom, palpitation, sleep deprivation, irritability, heartburn and tiredness,” as well as such objective measurements as their blood count, cholesterol, DNA damage, antioxidant status, and lung function. The amla extract used “showed a significant improvement compared to the placebo group in all the subjective and objective parameters tested with no reports of adverse events.” No side effects at all. That’s unbelievable! No, that’s unbelievable. And indeed, it’s completely not true.  

Yes, subjective complaints got better in the amla group, but they got better in the placebo group, too, with arbitrary scoring systems and no statistical analysis whatsoever. And, of the two dozen objective measures, only half could be said to reach any kind of before-and-after statistical significance and only three were significant enough to account for the fact that if you measure two dozen things, a few might pop up as positive if only by chance. Any time you see this kind of spin in the abstract, which is sometimes the only part of a study people read, you should suspect some kind of conflict of interest. However, no conflicts of interest were declared by the researchers, but that’s bullsh*t, as the study was funded by the very company selling those amla supplements! Sigh.

Anyway, one of those three significant findings was the Lp(a), so it might be worth a try in the context of a plant-based diet, which, in addition to helping with weight loss, can dramatically improve blood pressure (even after cutting down on blood pressure medications) and contribute to a 25-point drop in LDL cholesterol. Also, it may contribute to a 30 percent drop in C-reactive protein and significant reductions in other inflammatory markers for “a systemic, cardio-protective effect”—all thanks to this single dietary approach.

You may be interested in my video on Trans Fat in Meat and Dairy. Did you know that animal products are exempted from the ban? See Banning Trans Fat in Processed Foods but Not Animal Fat.

For more on amla and what else it can do, check out the related posts below.

If you missed my previous video on Lp(a), watch Treating High Lp(a)—A Risk Factor for Atherosclerosis. 

As I discuss in my video Treating High Lp(a): A Risk Factor for Atherosclerosis, Lp(a) is an “underestimated cardiovascular risk factor.” It causes coronary artery disease, heart attacks, strokes, peripheral arterial disease, calcified aortic valve disease, and heart failure. And these can occur in people who don’t even have high cholesterol—because Lp(a) is cholesterol, as you can see below and at 1:15 in my video. It’s an LDL cholesterol molecule linked to another protein, which, like LDL, transfers cholesterol into the lining of our arteries, contributing to the inflammation in atherosclerotic plaques. But “this increased risk caused by Lp(a) has not yet gained recognition by practicing physicians.” 

“The main reason for the limited clinical use of Lp(a) is the lack of effective and specific therapies to lower Lp(a) plasma levels.” Because “Lp(a) concentrations are approximately 90% genetically determined,” the conventional thinking has been you’re just kind of born with higher or lower levels and there isn’t much you can do about it. Even if that were the case, though, you might still want to know about it. If it were high, for instance, that would be all the more reason to make sure all the other risk factors that you do have more control over are as good as possible. It may help you quit smoking, for example, and motivate you to do everything you can to lower your LDL cholesterol as much as possible.  

Lp(a) levels in the blood can vary a thousand-fold between individuals, “from less than 0.1 mg/dL to as high as 387 mg/dL.” You can see a graph of the odds of heart disease at different levels in the graph below and at 2:20 in my video. Less than 20 mg/dL is probably optimal, with greater than 30 to 50 mg/dL considered to be elevated. Even when the more conservative threshold of greater than 50 mg/dL is used, that describes about 10 to 30 percent of the global population, an estimated 1.4 billion people. So, if we’re in the one in five people with elevated levels, what can we do about it? 

The way we know that Lp(a) causes atherosclerosis is that we can put it to the ultimate test. There is something called apheresis, which is essentially like a dialysis machine where they can take out your blood, wash out some of the Lp(a), and give your blood back to you. And when you do that, you can reverse the progression of the disease. As you can see in the graph below and at 3:06 in my video, atherosclerosis continues to get worse in the control group, but it gets better in the apheresis group. This is great for proving the role of Lp(a), but it has limited clinical application, given the “cost, limited access to centers, and the time commitment required for biweekly sessions of 2 to 4 h each.” 

It causes a big drop in blood levels, but they quickly creep back up, so you have to keep going in, as you can see in the graph below and at 3:26 in my video, costing more than $50,000 a year. 

There has to be a better way. We’ll explore the role diet can play, next.  

I’ve been wanting to do videos about Lp(a), but there just wasn’t much we could do about it until now. So, how do we lower Lp(a) with diet? Stay tuned for the exciting conclusion in my next video.

What can we do to minimize heart disease risk? My video How Not to Die from Heart Disease is a good starting point. 

“Approximately 90% of the world’s calories are provided by less than one percent of the known 250,000 edible plant species.” The big three are wheat, corn, and rice, and our reliance on them may be unsustainable, given the ongoing climate crisis. This has spurred new interest in “underutilized crops,” like quinoa, which might do better with drought and heat.

Quinoa has only recently been introduced into the Northern Hemisphere, but humans have been eating quinoa for more than 7,000 years. Is there any truth to its “superfood” designation, or is it all just marketing hooey?

Quinoa is a “pseudograin,” since the plant it comes from isn’t a type of grass. “Botanically speaking quinoa is an achene, a seed-like fruit with a hard coat,” and it has a lot of vitamins and minerals, but so do all whole grains. It also has a lot of protein. As you can see below and in a series of graphs starting at 1:05 in my video Benefits of Quinoa for Lowering Triglycerides, quinoa has more protein than other grains, but since when do we need more protein? Fiber is what we’re sorely lacking, and its fiber content is relatively modest, compared to barley or rye. Quinoa is pretty strong on folate and vitamin E, though, and it leads the pack on magnesium, iron, and zinc. So, it is nutritious, but when I think superfood, I think of something with some sort of special clinical benefit. Broccoli is a superfood, strawberries are a superfood, and so is garlic, but quinoa? Consumer demand is up, thanks in part to “perceived health benefits,” and it has all sorts of purported benefits in lab animals, but there have been very few human studies. 

The first trial was a before-and-after study of quinoa granola bars that showed drops in triglycerides and cholesterol, as you can see below and at 1:53 in my video, but it didn’t have a control group, so we don’t know how much of that would have happened without the quinoa. The kind of study I want to see is a randomized controlled trial. When researchers gave participants about a cup of cooked quinoa every day for 12 weeks, they experienced a 36 percent drop in their triglycerides. That’s comparable to what one gets with triglyceride-lowering drugs or high-dose fish oil supplements.

Which is better, regular quinoa or red quinoa? As you can see in the graph below and at 2:22 in my video, the red variety has about twice the antioxidant power, leading the investigators to conclude that red quinoa “might…contribute significantly to the management and/or prevention of degenerative diseases associated with free radical damage,” but it’s never been put to the test. 

What about black quinoa? Both red and black quinoa appear to be equally antioxidant-rich, both beating out the more conventional white variety, as you can see in the graph below and at 2:46 in my video. 

The only caveat I could find is to inform your doctor before your next colonoscopy or else they might mistake quinoa for parasites. As reported in a paper, a “colonoscopy revealed numerous egg-like tan-yellow ovoid objects, 2 to 3 mm in diameter, of unclear cause,” but they were just undigested quinoa.

For more on the superfoods I mentioned, check the related posts below.

Isn’t fish oil important to heart health? Find out in my video Is Fish Oil Just Snake Oil?.

When it comes to uncovering the root causes of the obesity epidemic, there appears to be manufactured confusion, “with major studies reasserting that the causes of obesity are ‘extremely complex’ and ‘fiendishly hard to untangle,’” but having just reviewed the literature, it doesn’t seem like much of a mystery to me.

It’s the food.

Attempts at obfuscation—rolling out hosts of “implausible explanations,” like sedentary lifestyles or lack of self-discipline—cater to food manufacturers and marketers more than the public’s health and our interest in the truth. “When asked about the role of restaurants in contributing to the obesity problem, Steven Anderson, president of the National Restaurant Association stated, “Just because we have electricity doesn’t mean you have to electrocute yourself.” Yes, but Big Food is effectively attaching electrodes to shock and awe the reward centers in our brains to undermine our self-control.

It is hard to eat healthfully against the headwind of such strong evolutionary forces. No matter what our level of nutrition knowledge, in the face of pepperoni pizza, “our genes scream, ‘Eat it now!’” Anyone who doubts the power of basic biological drives should see how long they can go without blinking or breathing. Any conscious decision to hold your breath is soon overcome by the compulsion to breathe. In medicine, shortness of breath is sometimes even referred to as “air hunger.” The battle of the bulge is a battle against biology, so obesity is not some moral failing. It’s not gluttony or sloth. It is a natural, “normal response, by normal people, to an abnormal situation”—the unnatural ubiquity of calorie-dense, sugary, and fatty foods.

The sea of excess calories we are now floating in (and some of us are drowning in) has been referred to as a “toxic food environment.” This helps direct focus away from the individual and towards the societal forces at work, such as the fact that the average child is blasted with 10,000 commercials for food a year. Or maybe I should say ads for pseudo food, as 95 percent are for “candy, fast food, soft drinks [aka liquid candy], and sugared cereals [aka breakfast candy].”

Wait a second, though. If weight gain is just a natural reaction to the easy availability of mountains of cheap, yummy calories, then why isn’t everyone fat? As you can see below and at 2:41 in my video The Role of the Toxic Food Environment in the Obesity Epidemic, in a certain sense, most everyone is. It’s been estimated that more than 90 percent of American adults are “overfat,” defined as having “excess body fat sufficient to impair health.” This can occur even “in those who are normal-weight and non-obese, often due to excess abdominal fat.

However, even if you look just at the numbers on the scale, being overweight is the norm. If you look at the bell curve and input the latest data, more than 70 percent of us are overweight. A little less than one-third of us is normal weight, on one side of the curve, and more than a third is on the other side, so overweight that we’re obese. You can see in the graph below and at 3:20 in my video.

If the food is to blame, though, why doesn’t everyone get fat? That’s like asking if cigarettes are really to blame, why don’t all smokers get lung cancer? This is where genetic predispositions and other exposures can weigh in to tip the scales. Different people are born with a different susceptibility to cancer, but that doesn’t mean smoking doesn’t play a critical role in exploding whatever inherent risk you have. It’s the same with obesity and our toxic food environment. It’s like the firearm analogy: Genes may load the gun, but diet pulls the trigger. We can try to switch the safety back on with smoking cessation and a healthier diet.

What happened when two dozen study participants were given the same number of excess calories? They all gained weight, but some gained more than others. Overfeeding the same 1,000 calories a day, 6 days a week for 100 days, caused weight gains ranging from about 9 pounds up to 29 pounds. The same 84,000 extra calories caused different amounts of weight gain. Some people are just more genetically susceptible. The reason we suspect genetics is that the 24 people in the study were 12 sets of identical twins, and the variation in weight gain between each of them was about a third less. As you can see in the graph below and at 4:41 in my video, a similar study with weight loss from exercise found a similar result. So, yes, genetics play a role, but that just means some people have to work harder than others. Ideally, inheriting a predisposition for extra weight gain shouldn’t give a reason for resignation, but rather motivation to put in the extra effort to unseal your fate. 

Advances in processing and packaging, combined with government policies and food subsidy handouts that fostered cheap inputs for the “food industrial complex,” led to a glut of ready-to-eat, ready-to-heat, ready-to-drink hyperpalatable, hyperprofitable products. To help assuage impatient investors, marketing became even more pervasive and persuasive. All these factors conspired to create unfettered access to copious, convenient, low-cost, high-calorie foods often willfully engineered with chemical additives to make them hyperstimulatingly sweet or savory, yet only weakly satiating. 

As we all sink deeper into a quicksand of calories, more and more mental energy is required to swim upstream against the constant “bombardment of advertising” and 24/7 panopticons of tempting treats. There’s so much food flooding the market now that much of it ends up in the trash. Food waste has progressively increased by about 50 percent since the 1970s. Perhaps better in the landfills, though, than filling up our stomachs. Too many of these cheap, fattening foods prioritize shelf life over human life.

But dead people don’t eat. Don’t food companies have a vested interest in keeping their consumers healthy? Such naiveté reveals a fundamental misunderstanding of the system. A public company’s primary responsibility is to reap returns for its investors. “How else could we have tobacco companies, who are consummate marketers, continuing to produce products that kill one in two of their most loyal customers?” It’s not about customer satisfaction, but shareholder satisfaction. The customer always comes second.

Just as weight gain may be a perfectly natural reaction to an obesogenic food environment, governments and businesses are simply responding normally to the political and economic realities of our system. Can you think of a single major industry that would benefit from people eating more healthfully? “Certainly not the agriculture, food product, grocery, restaurant, diet, or drug industries,” wrote emeritus professor Marion Nestle in a Science editorial when she was chair of nutrition at New York University. “All flourish when people eat more, and all employ armies of lobbyists to discourage governments from doing anything to inhibit overeating.”

If part of the problem is cheap tasty convenience, is hard-to-find food that’s gross and expensive the solution? Or might there be a way to get the best of all worlds—easy, healthy, delicious, satisfying meals that help you lose weight? That’s the central question of my book How Not to Diet. Check it out for free at your local library.

This is it—the final video in this 11-part series. If you missed any of the others, see the related posts below. 

The plague of tobacco deaths wasn’t due just to the mass manufacturing and marketing of cheap cigarettes. Tobacco companies actively sought to make their products even more crave-able by spraying sheets of tobacco with nicotine and additives like ammonia to provide “a bigger nicotine ‘kick.’” Similarly, taste engineers are hired by the food industry to maximize product irresistibility.

Taste is the leading factor in food choice. “Sugar, fat, and salt have been called the three points of the compass” to produce “superstimulating” and “hyper palatability” to tempt people into impulsive buys and compulsive consumption. Foods are intentionally designed to hook into our evolutionary triggers and breach whatever biological barriers help “keep consumption within reasonable limits.”

Big Food is big business. The processed food industry alone brings in more than $2 trillion a year. That affords them the economic might to manipulate not only taste profiles, but public policy and scientific inquiry, too. The food, alcohol, and tobacco industries have all used similar unsavory tactics: blocking health regulations, co-opting professional organizations, creating front groups, and distorting the science. The common “corporate playbook” shouldn’t be surprising, given the common corporate threads. At one time, for example, tobacco giant Philip Morris owned both Kraft and Miller Brewing.

As you can see below and at 1:45 in my video The Role of Corporate Influence in the Obesity Epidemic, in a single year, the food industry spent more than $50 million to hire hundreds of lobbyists to influence legislation. Most of these lobbyists were “revolvers,” former federal employees in the revolving door between industry and its regulators, who could push corporate interests from the inside, only to be rewarded with cushy lobbying jobs after their “public service.” In the following year, the industry acquired a new weapon—a stick to go along with all those carrots. On January 21, 2010, the Supreme Court’s five-to-four Citizen’s United ruling permitted corporations to spend unlimited amounts of money on campaign ads to trash anyone who dared stand against them. No wonder our elected officials have so thoroughly shrunk from the fight, leaving us largely with a government of Big Food, by Big Food, and for Big Food. 

Globally, a similar dynamic exists. Weak tea calls from the public health community for voluntary standards are met not only with vicious fights against meaningful change but also massive transnational trade and foreign investment deals that “cement the protection of their [food industry] profits” into the laws of the lands.

The corrupting commercial influence extends to medical associations. Reminiscent of the “just what the doctor ordered” cigarette ads of yesteryear, as you can see below and at 3:05 in my video, the American Academy of Family Physicians accepted millions from The Coca-Cola Company to “develop consumer education content on beverages and sweeteners.” 

On the front line, fake grassroots “Astroturf” groups are used to mask the corporate message. RJ Reynolds created Get Government Off Our Back (memorably acronymed GGOOB), “a front group created by the tobacco industry to fight regulation,” for instance. Americans Against Food Taxes may as just as well be called “Food Industry Against Food Taxes.” The power of front group formation is enough to bind bitter corporate rivals; the Sugar Association and the Corn Refiners Association linked arms with the National Confectioners Association to partner with Americans for Food and Beverage Choice.

Using another tried-and-true tobacco tactic, research front groups can be used to subvert the scientific process by shaping or suppressing the science that deviates from the corporate agenda. Take the trans fat story. Food manufacturers have not only “long denied that trans fats were associated with disease,” but actively “worked to limit research on trans fats” and “discredit potentially damaging findings.”

At what cost? The global death toll from foods high in trans fat, saturated fat, salt, and sugar is at 14 million lost lives every year. The inability of countries around the world to turn the tide on obesity “is not a failure of individual will-power. This is a failure of political will to take on big business,” said the Director-General of the World Health Organization. “It is a failure of political will to take on the powerful food and soda industries.” She ended her keynote address before the National Academy of Medicine entitled “Obesity and Diabetes: The Slow-Motion Disaster” with these words: “The interests of the public must be prioritized over those of corporations.”

Are you mad yet? To sum up my answer to the question underlying my What Triggered the Obesity Epidemic? webinar, it’s the food. I close next with my wrap-up video: The Role of the Toxic Food Environment in the Obesity Epidemic. 

This was part of an 11-part series. See the related posts below.

If the political angle interests you, check out: 

• Big Food Using the Tobacco Industry Playbook
• How Smoking in 1959 Is Like Eating in 2019
• Sugar Industry Attempts to Manipulate the Science
• The Food Industry Wants the Public Confused About Nutrition
• A Political Lesson on the Power of the Food Industry 

Food and beverage companies frame body weight as “a matter of personal choice.” Even when we aren’t distracted, the power of the “eat more” food environment may sometimes overcome our conscious controls of overeating. One look around the room at a dietician convention can tell you that even nutrition professionals are vulnerable to the aggressively marketed ubiquity of tasty, cheap, convenient calories. This suggests there are aspects of our eating behaviors “that defy personal insight or are below individual awareness,” flying below the radar of conscious awareness. Appetite physiologists call the result of these subconscious actions “passive overconsumption.”

Remember that brain scan study where the thought of a milkshake lit up the same reward pathways in the brain as substance abuse? That was triggered just by a picture of a milkshake. Dopamine gets released, cravings get activated, and we’re motivated to eat. Intellectually, we know it’s just an image, but our lizard brain sees survival. It’s just a reflexive response over which we have little control, which is why marketers ensure there are pictures of milkshakes and their equivalents everywhere.

As I discuss in my video The Role of Personal Responsibility in the Obesity Epidemic, maintaining a balance between calories in and calories out feels like a series of voluntary acts under conscious control, but it may be more akin to bodily functions, such as blinking, breathing, coughing, swallowing, or sleeping. You can try to will yourself power over any of these, but by and large, they just happen automatically, driven by ancient scripts.

Not only are food ads ubiquitous, but so is the food. The types of establishments selling food products expanded dramatically in the 1970s and 1980s. Now, you can find candy and snacks at the checkout counters of “gasoline stations, building material outlets, auto parts stores, drug stores, and home furnishing stores” and more. The largest food retailer in the United States is Wal-Mart. You can get that jolt of “dopamine and the associated artificially induced feelings of hunger in modern society” around every turn. Every day, we run the gauntlet.

It’s also become “socially acceptable to eat food at any time of day and anywhere—in cars, in your hand, on the street—places where eating had never been acceptable.” We’ve become a snacking society. Vending machines are everywhere. Daily eating episodes seem to have gone up by about a quarter since the late 1970s, increasing from about four to five occasions a day, potentially accounting for twice the calorie increase attributed to increasing portion sizes. Snacks and beverages alone could account for the bulk of the calorie surplus implicated in the obesity epidemic.

And think of the children. Here we are trying to do the best for our kids, role-modeling healthy habits and feeding them healthy foods, but then they venture out into a veritable tornado of junky food and manipulative messages. A commentary in The New England Journal of Medicine asked: “But why should Mr. and Ms. G.’s efforts to protect their children from life-threatening illness be undermined by massive marketing campaigns from the manufacturers of junk food?” Pediatricians are now encouraged to have the “French Fry Discussion” with parents at the 12-month well-child visit instead of waiting until their kids are two—though even that may be too late. As you can see below and at 3:35 in my video, two-thirds of infants are being fed junk food by their first birthday. 

Dr. David Katz may have said it best in the Harvard Health Policy Review: “Those who contend that parental or personal responsibility should carry the day despite these environmental temptations might consider the implications of generalizing the principle. Perhaps children should be encouraged, but not required, to attend school and tempted each morning by alternatives, such as buses to the circus, zoo, or beach.” 

It may be helpful to take a step back and think of what’s at stake here. We aren’t just talking about being manipulated into buying a different brand of toothpaste. The obesity pandemic has resulted in millions of deaths and untold suffering. If you aren’t mad yet, brace yourself for my next video: The Role of Corporate Influence in the Obesity Epidemic.

This is the ninth video in my 11-part series. If you missed any of the previous ones, see the related posts below.

The opening words of the Institute of Medicine’s report on the potential threat posed by food ads were: “Marketing works.” Certainly, there is a “large number of well-conducted randomized experiments” I could go through with you that “have shown that exposure to marketing—especially, but not only, advertising—changes people’s eating behavior. Marketing causes people to choose to eat more.” But, what do you need to know beyond the fact that the industry spends tens of billions of dollars a year on it? To get people to drink its brown sugar water, do you think Coca-Cola would spend a penny more than it thought it had to? It’s like when my medical colleagues accept “drug lunches” from pharmaceutical representatives and take offense that I would suggest it might affect their prescribing practices. Do they really think drug companies are in the business of giving away free money for nothing? They wouldn’t do it if it didn’t work. 

To give you a sense of marketing’s insidious nature, let me share an interesting piece of research published in the world’s leading scientific journal: “In-Store Music Affects Product Choice” documented an experiment in which French accordion music or German Bierkeller music was played on alternate days in the wine section of a grocery store. As you can see below and at 1:27 in my video The Role of Food Advertisements in the Obesity Epidemic, on the days the French music played in the background, people were three times more likely to buy French wine, and on German music days, shoppers were about three times more likely to buy German wine. And it wasn’t a difference of just a few percent; it was a complete three-fold reversal. Despite the dramatic effect, when shoppers were approached afterward, the vast majority of them denied the music had influence on their choice. 

Most of our day-to-day behavior does not appear to be dictated by careful, considered deliberations, even if we’d like to think that were the case. Rather, we tend to make more automatic, impulsive decisions triggered by unconscious cues or habitual patterns, especially when we are “under stress, tired, or preoccupied. This unconscious part of our brain is estimated to function and guide our behaviors at least 95% of the time.” This is the arena where marketing manipulations do most of their dirty work. 

The part of our brain that governs conscious awareness may only be able to process about 50 bits of information per second, which is roughly equivalent to a short tweet. Our entire cognitive capacity, on the other hand, is estimated to process more than 10 million bits per second. Because we’re only able to purposefully process a limited amount of information at a time, if we’re distracted or otherwise unable to concentrate, our decisions can become even more impulsive. An elegant illustration of this “cognitive overload” effect was provided from an experiment involving fruit salad and chocolate cake.

Before calls could be made at the touch of a button or the sound of our voice, the seven-digit span of phone numbers in the United States was based in part on the longest sequence most people can recall on the fly. We only seem to be able to hold about seven chunks of information (plus or minus two) in our immediate short-term memory. The study’s setup: Randomize people to memorize either a seven-digit number or a two-digit number to be recalled in another room down the hall. On the way, offer them the choice of a fruit salad or a piece of chocolate cake. Memorizing a two-digit number is easy and presumably takes few cognitive resources. As you can see in the graph below and at 3:52 in my video, under the two-digit condition, most study participants chose fruit salad. Faced with the same decision, most of those trying to keep seven digits in their heads just went for the cake. 

This can play out in the real world by potentiating the effect of advertising. Have people watch a TV show with commercials for unhealthy snacks, and, no surprise, they eat more unhealthy snacks compared to those exposed to non-food ads. Or maybe that is a surprise. We all like to think we’re in control and not so easily manipulated. The kicker, though, is that we may be even more susceptible the less we pay attention. Randomize people to the same two-digit or seven-digit memorization task during the TV show, and the snack-attack effect was magnified among those who were more preoccupied. How many of us have the TV on in the background or multi-task during commercial breaks? Research suggests that may make us even more impressionable to the subversion of our better judgment. 

There’s an irony in all of this. Calls for restrictions on marketing are often resisted by invoking the banner of freedom. What does that even mean in this context, when research shows how easily our free choices can be influenced without our conscious control? A senior policy researcher at the RAND Corporation even went as far as to suggest that, given the dire health consequences of our unhealthy eating habits, “the marketing techniques of which we are unaware should be considered in the same light as the invisible carcinogens and toxins in the air and water that can poison us without our awareness.”

Given the role marketing can play even when we least suspect it, what is the role of personal responsibility in the obesity epidemic? That’s the subject of my next video.

We are winding down this series on obesity, with three videos remaining: 

• The Role of Personal Responsibility in the Obesity Epidemic 
• The Role of Corporate Influence in the Obesity Epidemic 
• The Role of the Toxic Food Environment in the Obesity Epidemic 

 If you missed any of the previous videos, see the related posts below. 

In the 1970s, the U.S. government went from just subsidizing some of the worst foods to paying companies to make more of them: “Congress passed laws reversing long-standing farm policies aimed at protecting prices by limiting production” and started giving payouts in proportion to output. Extra calories started pouring into the food supply.

Then Jack Welch gave a speech. In 1981, the CEO of General Electric effectively launched the “shareholder value movement,” reorienting the primary goal of corporations towards maximizing short-term returns for investors. This placed extraordinary pressure from Wall Street on food companies to post increasing profit growth every quarter to boost their share price. There was already a glut of calories on the market and now they had to sell even more.

This placed food and beverage CEOs in an impossible bind. It’s not like they’re rubbing their sticky hands together at the thought of luring more Hansels and Gretels to their doom in their houses of candy. Food giants couldn’t do the right thing even if they wanted. They are beholden to investors. If they stopped marketing to kids or tried to sell healthier food or did anything else that could jeopardize their quarterly profit growth, Wall Street would demand a change in management. Healthy eating is bad for business. It’s not some grand conspiracy; it’s not even anyone’s fault. It’s just how the system works.

As I discuss in my video The Role of Marketing in the Obesity Epidemic, given the constant demands for corporate growth and rapid returns in an already oversaturated marketplace, the food industry needed to get people to eat more. Like the tobacco industry before them, it turned to the ad makers. The food industry spends about $10 billion a year on advertising and around another $20 billion on other forms of marketing, such as trade shows, consumer promotions, incentives, and supermarket “slotting fees.” Food and beverage companies purchase shelf space from supermarkets to prominently display their most profitable products. They pay supermarkets. The practice is also known as “cliffing,” because companies “force suppliers to bid against each other for shelf space with the loser pushed ‘over the cliff.’” With slotting fees costing up to $20,000 per item, per retailer, and per city, you can imagine what types of foods get the special treatment. Hint: It ain’t broccoli.

To get a sense of what kind of products merit prime shelf real estate, look no further than the checkout aisle. “Merchandising the power categories on every lane is critical,” reads a trade publication on the “best practices for superior checkout merchandising.” It was referring to candy bars and beverages. Just a 1 percent power category boost in sales could earn a store an extra $15,000 a year. It’s not that publicly traded companies don’t care about their customers’ health. They might, but like most of the leading grocery store chains, their “primary fiduciary responsibility is to increase profits” above other considerations.

For instance, tens of millions of dollars are spent annually advertising a single brand of candy bar. McDonald’s alone may spend billions a year. Now, “the food industry is the biggest spender on advertising of any major sector of the economy.”

“Reagan-era deregulatory policies removed limits on television marketing of food products to children.” Now, the average child may see more than 10,000 TV food ads a year, and that’s on top of “the marketing content online, in print, at school, at the movies, in video games, or at school,” or even on their phones. “Nearly all food marketing to children worldwide promotes products that can adversely affect their health.”

Besides the massive early exposure and ubiquity, food marketing has become “highly sophisticated. With the help of child psychologists, companies began to understand the factors that unconsciously influenced sales. They found out, for example, how to influence children and get them to manipulate their parents.” Packaging was designed to best attract a child’s attention, and then those products are placed at their eye level in the store. You know those mirrored bubbles in the ceilings of supermarkets? They aren’t just for shoplifters. Closed-circuit cameras and GPS-like devices on shopping carts are used to strategize how best to guide shoppers toward the market’s most profitable products. Behavioral psychology is widely applied to increase impulse buying, and eye movement tracking technologies are utilized.

The “unprecedented expansion in the scope, power, and ubiquity of food marketing…coincided with an unprecedented expansion in food consumption in predictable ways.” Some techniques have “skyrocket[ed] from essentially zero to multi-billion-dollar industries” since the 1980s, including “product placement, in-school advertising, event sponsorships.” This led one noted economist to conclude that “the most compelling single interpretation of the admittedly incomplete data we have is that the large increase in obesity is due to marketing.” Yes, innovations in manufacturing and political maneuvering led to a food supply bursting at the seams with close to 4,000 calories a day for us all, but it’s the advances in marketing manipulations that try to peddle that surplus into our mouths. 

I think the natural reaction to the suggestion of the power of marketing is: I’m too smart to fall for that. Marketing works on other people, but I can see through it. But that’s what everyone thinks! For a splash of cold water to shake us all out of this delusion, I next bring you some data: The Role of Food Advertisements in the Obesity Epidemic. 

Also, for both the role of marketing and food advertisements, check out Friday Favorites: The Role of Marketing and Food Advertisements in the Obesity Epidemic.

This is the seventh in an 11-video series. If you missed any of the first six, check out the related posts below. 

The rise in calorie surplus sufficient to explain the obesity epidemic was less a change in food quantity than in food quality. Access to cheap, high-calorie, low-quality convenience foods exploded, and the federal government very much played a role in making this happen. U.S. taxpayers give billions of dollars in subsidies to prop up the likes of the sugar industry, the corn industry and its high-fructose syrup, and the production of soybeans, about half of which is processed into vegetable oil and the other half is used as cheap feed to help make dollar-menu meat. You can see a table of subsidy recipients below and at 0:49 in my video The Role of Taxpayer Subsidies in the Obesity Epidemic. Why do taxpayers give nearly a quarter of a billion dollars a year to the sorghum industry? When was the last time you sat down to some sorghum? It’s almost all fed to cattle and other livestock. “We have created a food price structure that favors relatively animal source foods, sweets, and fats”—animal products, sugars, and oils.

The Farm Bill started out as an emergency measure during the Great Depression of the 1930s to protect small farmers but was weaponized by Big Ag into a cash cow with pork barrel politics—including said producers of beef and pork. From 1970 to 1994, global beef prices dropped by more than 60 percent. And, if it weren’t for taxpayers “sweetening the pot” with billions of dollars a year, high-fructose corn syrup would cost the soda industry about 12 percent more. Then we hand Big Soda billions more through the Supplemental Nutrition Assistance Program (SNAP), formerly known as the Food Stamps Program, to give sugary drinks to low-income individuals. Why is chicken so cheap? After one Farm Bill, corn and soy were subsidized below the cost of production for cheap animal fodder. We effectively handed the poultry and pork industries about $10 billion each. That’s not chicken feed—or rather, it is! 

This is changing what we eat. 

As you can see below and at 2:03 in my video, thanks in part to subsidies, dairy, meats, sweets, eggs, oils, and soda were all getting relatively cheaper compared to the overall consumer food price index as the obesity epidemic took off, whereas the relative cost of fresh fruits and vegetables doubled. This may help explain why, during about the same period, the percentage of Americans getting five servings of fruits and vegetables a day dropped from 42 percent to 26 percent. Why not just subsidize produce instead? Because that’s not where the money is. 

“To understand what is shaping our foodscape today, it is important to understand the significance of differential profit.” Whole foods or minimally processed foods, such as canned beans or tomato paste, are what the food business refers to as “commodities.” They have such slim profit margins that “some are typically sold at or below cost, as ‘loss leaders,’ to attract customers to the store” in the hopes that they’ll also buy the “value-added” products. Some of the most profitable products for producers and vendors alike are the ultra-processed, fatty, sugary, and salty concoctions of artificially flavored, artificially colored, and artificially cheap ingredients—thanks to taxpayer subsidies. 

Different foods reap different returns. Measured in “profit per square foot of selling space” in the supermarket, confectionaries like candy bars consistently rank among the most lucrative. The markups are the only healthy thing about them. Fried snacks like potato chips and corn chips are also highly profitable. PepsiCo’s subsidiary Frito-Lay brags that while its products represented only about 1 percent of total supermarket sales, they may account for more than 10 percent of operating profits for supermarkets and 40 percent of profit growth. 

It’s no surprise, then, that the entire system is geared towards garbage. The rise in the calorie supply wasn’t just more food but a different kind of food. There’s a dumb dichotomy about the drivers of the obesity epidemic: Is it the sugar or the fat? They’re both highly subsidized, and they both took off. As you can see below and at 4:29 and 4:35 in my video, along with a significant rise in refined grain products that is difficult to quantify, the rise in obesity was accompanied by about a 20 percent increase in per capita pounds of added sugars and a 38 percent increase in added fats. 

More than half of all calories consumed by most adults in the United States were found to originate from these subsidized foods, and they appear to be worse off for it. Those eating the most had significantly higher levels of chronic disease risk factors, including elevated cholesterol, inflammation, and body weight. 

If it really were a government of, by, and for the people, we’d be subsidizing healthy foods, if anything, to make fruits and vegetables cheap or even free. Instead, our tax dollars are shoveled to the likes of the sugar industry or to livestock feed to make cheap, fast-food meat. 

Speaking of sorghum, I had never had it before and it’s delicious! In fact, I wish I had discovered it before How Not to Diet was published. I now add sorghum and finger millet to my BROL bowl which used to just include purple barley groats, rye groats, oat groats, and black lentils, so the acronym has become an unpronounceable BROLMS. Anyway, sorghum is a great rice substitute for those who saw my rice and arsenic video series and were as convinced as I am that we need to diversify our grains. 

We now turn to marketing. After all of the taxpayer-subsidized glut of calories in the market, the food industry had to find a way to get it into people’s mouths. So, next: The Role of Marketing in the Obesity Epidemic. 

We’re about halfway through this series on the obesity epidemic. If you missed any so far, check out the related videos below.

The rise in the number of calories provided by the food supply since the 1970s “is more than sufficient to explain the US epidemic of obesity.” Similar spikes in calorie surplus were noted in developed countries around the world in parallel with and presumed to be primarily responsible for, the expanding waistlines of their populations. After taking exports into account, by the year 2000, the United States was producing 3,900 calories for every man, woman, and child—nearly twice as much as many people need. 

It wasn’t always this way. The number of calories in the food supply actually declined over the first half of the twentieth century and only started its upward climb to unprecedented heights in the 1970s. The drop in the first half of the century was attributed to the reduction in hard manual labor. The population had decreased energy needs, so they ate decreased energy diets. They didn’t need all the extra calories. But then the “energy balance flipping point” occurred, when the “move less, stay lean phase” that existed throughout most of the century turned into the “eat more, gain weight phase” that plagues us to this day. So, what changed?

As I discuss in my video The Role of Processed Foods in the Obesity Epidemic, what happened in the 1970s was a revolution in the food industry. In the 1960s, most food was prepared and cooked in the home. The typical “married female, not working” spent hours a day cooking and cleaning up after meals. (The “married male, non-working spouse” averaged nine minutes, as you can see below and at 1:34 in my video.) But then a mixed-blessing transformation took place. Technological advances in food preservation and packaging enabled manufacturers to mass prepare and distribute food for ready consumption. The metamorphosis has been compared to what happened a century before with the mass production and supply of manufactured goods during the Industrial Revolution. But this time, they were just mass-producing food. Using new preservatives, artificial flavors, and techniques, such as deep freezing and vacuum packaging, food corporations could take advantage of economies of scale to mass produce “very durable, palatable, and ready-to-consume” edibles that offer “an enormous commercial advantage over fresh and perishable whole or minimally processed foods.” 

Think ye of the Twinkie. With enough time and effort, “ambitious cooks” could create a cream-filled cake, but now they are available around every corner for less than a dollar. If every time someone wanted a Twinkie, they had to bake it themselves, they’d probably eat a lot fewer Twinkies. The packaged food sector is now a multitrillion-dollar industry.

Consider the humble potato. We’ve long been a nation of potato eaters, but we usually baked or boiled them. Anyone who’s made fries from scratch knows what a pain it is, with all the peeling, cutting, and splattering of oil. But with sophisticated machinations of mechanization, production became centralized and fries could be shipped at -40°F to any fast-food deep-fat fryer or frozen food section in the country to become “America’s favorite vegetable.” Nearly all the increase in potato consumption in recent decades has been in the form of french fries and potato chips. 

Cigarette production offers a compelling parallel. Up until automated rolling machines were invented, cigarettes had to be rolled by hand. It took 50 workers to produce the same number of cigarettes a machine could make in a minute. The price plunged and production leapt into the billions. Cigarette smoking went from being “relatively uncommon” to being almost everywhere. In the 20th century, the average per capita cigarette consumption rose from 54 cigarettes a year to 4,345 cigarettes “just before the first landmark Surgeon General’s Report” in 1964. The average American went from smoking about one cigarette a week to half a pack a day.

Tobacco itself was just as addictive before and after mass marketing. What changed was cheap, easy access. French fries have always been tasty, but they went from being rare, even in restaurants, to being accessible around each and every corner (likely next to the gas station where you can get your Twinkies and cigarettes).

The first Twinkie dates back to 1930, though, and Ore-Ida started selling frozen french fries in the 1950s. There has to be more to the story than just technological innovation, and we’ll explore that next.

This explosion of processed junk was aided and abetted by Big Government at the behest of Big Food, which I explore in my video The Role of Taxpayer Subsidies in the Obesity Epidemic.

This is the fifth video in an 11-part series. Here are the first four: 

• The Role of Diet vs. Exercise in the Obesity Epidemic 
• The Role of Genes in the Obesity Epidemic 
• The Thrifty Gene Theory: Survival of the Fattest 

• Cut the Calorie-Rich-And-Processed Foods 

Videos still to come are listed in the related videos below.

The traditional medical view on obesity, as summed up nearly a century ago: “All obese persons are, alike in one fundamental respect,—they literally overeat.” While this may be true in a technical sense, it is in reference to overeating calories, not food. Our primitive urge to overindulge is selective. People don’t tend to lust for lettuce. We have a natural inborn preference for sweet, starchy, or fatty foods because that’s where the calories are concentrated.

Think about hunting and gathering efficiency. We used to have to work hard for our food. Prehistorically, it didn’t make sense to spend all day collecting types of food that on average don’t provide at least a day’s worth of calories. You would have been better off staying back at the cave. So, we evolved to crave foods with the biggest caloric bang for their buck.

If you were able to steadily forage a pound of food an hour and it had 250 calories per pound, it might take you ten hours just to break even on your calories for the day. But if you were gathering something with 500 calories a pound, you could be done in five hours and spend the next five working on your cave paintings. So, the greater the energy density—that is, the more calories per pound—the more efficient the foraging. We developed an acute ability to discriminate foods based on calorie density and to instinctively desire the densest.

If you study the fruit and vegetable preferences of four-year-old children, what they like correlates with calorie density. As you can see in the graph below and at 1:52 in my video Friday Favorites: Cut the Calorie-Rich-And-Processed Foods, they prefer bananas over berries and carrots over cucumbers. Isn’t that just a preference for sweetness? No, they also prefer potatoes over peaches and green beans over melon, just like monkeys prefer avocados over bananas. We appear to have an inborn drive to maximize calories per mouthful. 

All the foods the researchers tested in the study with four-year-old kids naturally had less than 500 calories per pound. (Bananas topped the chart at about 400.) Something funny happens when you start going above that: We lose our ability to differentiate. Over the natural range of calorie densities, we have an uncanny aptitude to pick out the subtle distinctions. However, once you start heading towards bacon, cheese, and chocolate territory, which can reach thousands of calories per pound, our perceptions become relatively numb to the differences. It’s no wonder since these foods were unknown to our prehistoric brains. It’s like the dodo bird failing to evolve a fear response because they had no natural predators—and we all know how that turned out—or sea turtle hatchlings crawling in the wrong direction towards artificial light rather than the moon. It is aberrant behavior explained by an “evolutionary mismatch.”

The food industry exploits our innate biological vulnerabilities by stripping crops down into almost pure calories—straight sugar, oil (which is pretty much pure fat), and white flour (which is mostly refined starch). It also removes the fiber, because that effectively has zero calories. Run brown rice through a mill to make white rice, and you lose about two-thirds of the fiber. Turn whole-wheat flour into white flour, and lose 75 percent. Or you can run crops through animals (to make meat, dairy, and eggs) and remove 100 percent of the fiber. What you’re left with is CRAP—an acronym used by one of my favorite dieticians, Jeff Novick, for Calorie-Rich And Processed food.

Calories are condensed in the same way plants are turned into addictive drugs like opiates and cocaine: “distillation, crystallization, concentration, and extraction.” They even appear to activate the same reward pathways in the brain. Put people with “food addiction” in an MRI scanner and show them a picture of a chocolate milkshake, and the areas that light up in their brains (as you can see below and at 4:15 in my video) are the same as when cocaine addicts are shown a video of crack smoking. (See those images below and at 4:18 in my video.) 

“Food addiction” is a misnomer. People don’t suffer out-of-control eating behaviors to food in general. We don’t tend to compulsively crave carrots. Milkshakes are packed with sugar and fat, two of the signals to our brain of calorie density. When people are asked to rate different foods in terms of cravings and loss of control, most incriminated was a load of CRAP—highly processed foods like donuts, along with cheese and meat. Those least related to problematic eating behaviors? Fruits and vegetables. Calorie density may be the reason people don’t get up in the middle of the night and binge on broccoli.

Animals don’t tend to get fat when they are eating the foods they were designed to eat. There is a confirmed report of free-living primates becoming obese, but that was a troop of baboons who stumbled across the garbage dump at a tourist lodge. The garbage-feeding animals weighed 50 percent more than their wild-feeding counterparts. Sadly, we can suffer the same mismatched fate and become obese by eating garbage, too. For millions of years, before we learned how to hunt, our biology evolved largely on “leaves, roots, fruits, and nuts.” Maybe it would help if we went back to our roots and cut out the CRAP. 

A key insight I want to emphasize here is the concept of animal products as the ultimate processed food. Basically, all nutrition grows from the ground: seeds, sunlight, and soil. That’s where all our vitamins come from, all our minerals, all the protein, all the essential amino acids. The only reason there are essential amino acids in a steak is because the cow ate them all from plants. Those amino acids are essential—no animals can make them, including us. We have to eat plants to get them. But we can cut out the middlemoo and get nutrition directly from the Earth, and, in doing so, get all the phytonutrients and fiber that are lost when plants are processed through animals. Even ultraprocessed junk foods may have a tiny bit of fiber remaining, but all is lost when plants are ultra-ultraprocessed through animals.

Having said that, there was also a big jump in what one would traditionally think of as processed foods, and that’s the video we turn to next: The Role of Processed Foods in the Obesity Epidemic.

We’re making our way through a series on the cause of the obesity epidemic. So far, we’ve looked at exercise (The Role of Diet vs. Exercise in the Obesity Epidemic) and genes (The Role of Genes in the Obesity Epidemic and The Thrifty Gene Theory: Survival of the Fattest), but, really, it’s the food.

If you’re familiar with my work, you know that I recommend eating a variety of whole plant foods, as close as possible to the way nature intended. I capture this in my Daily Dozen, which you can download for free here or get the free app (iTunes and Android). On the app, you’ll see that there’s also an option for those looking to lose weight: my 21 Tweaks. But before you go checking them off, be sure to read about the science behind the checklist in my book How Not to Diet. Get it for free at your local public library. If you choose to buy a copy, note that all proceeds from all of my books go to charity. 

It’s been said that “Nothing in biology makes sense except in the light of evolution.” The known genetic contribution to obesity may be small, but, in a certain sense, you could argue that it’s all in our genes. The excess consumption of available calories may be hardwired into our DNA. We were born to eat.

Throughout human history and beyond, we existed in survival mode—in unpredictable scarcity. We’ve been programmed with a powerful drive to eat as much as we can while we can and just store the rest for later. Food availability could never be taken for granted, so those who ate more at the moment and were best able to store more fat for the future might better survive subsequent shortages to pass along their genes. So, generation after generation, millennia after millennia, those with lesser appetites may have died out, while those who gorged may have selectively lived long enough to pass along their genetic predisposition to eat and store more calories. That may be how we evolved into such voracious calorie-conserving machines. Now that we’re no longer living in such lean times, though, we’re no longer so lean ourselves.

What I just described is the “thrifty gene” concept proposed in 1962. As I discuss in my video The Thrifty Gene Theory: Survival of the Fattest, it suggests that obesity is the result of a “‘mismatch’ between the environment in which humans evolved and our modern environment”—like being a polar bear in a jungle. All that fur and fat may have given polar bears an edge in the Arctic but would be decidedly disadvantageous in the Congo. Similarly, a propensity to pack on the pounds may have been a plus in prehistoric times but can turn into a liability when our scarcity-sculpted biology is plopped down into the land of plenty. So, it’s not gluttony or sloth. Obesity may simply be “a normal response to an abnormal environment.”

Much of our physiology is finely tuned to stay within a narrow range of upper and lower limits. If we get too hot, we sweat; if we get too cold, we shiver. Our body has mechanisms to keep us in balance. In contrast, our bodies have had little reason to develop an upper limit to the accumulation of body fat. In the beginning, there may have been evolutionary pressures to keep lithe and nimble in the face of predation, but thanks to things like weapons and fire, we haven’t had to outrun as many saber-toothed tigers for about two million years or so. This may have left our genes with the one-sided selection pressures to binge on every morsel in sight and stockpile as many calories as possible in our bodies.

What was once adaptive is now a problem—or at least so says the thrifty gene hypothesis that originated more than half a century ago. It “provides a simple and elegant explanation for the modern obesity epidemic and was quickly embraced by scientists and lay people alike.” Although the researcher, James Neel, later distanced himself from the original proposal, the basic premise, despite remaining mostly theoretical, is still “largely accepted” by the scientific community, and the implications are profound.

In 2013, the American Medical Association voted to classify obesity as a disease (going against the advice of its own Council on Science and Public Health). Not that it necessarily matters what we call it, but disease implies dysfunction. Bariatric drugs and surgery are not correcting an anomaly in human physiology. Our bodies are just doing what they were designed to do in the face of excess calories. Rather than being some sort of disorder, weight gain is largely “a normal response by normal people to an abnormal environment.” As you can see below and at 4:12 in my video, more than 70 percent of Americans are now overweight. It’s normal. 

“A body gaining weight when excess calories are available for consumption is behaving normally. Efforts to curtail such weight gain with drugs [or surgery] are not efforts to correct an anomaly in human physiology, but rather to deconstruct and reconstruct its normal operations at the core.”

If weight gain is largely a normal response by normal people to an abnormal situation, what exactly is that abnormal situation? Calorie-Rich-And-Processed Foods. (I’ll let you work out the acronym.) That’s the topic we’ll turn to next.

This is the third in an 11-video series on the history of the obesity epidemic. If you missed the first two, see The Role of Diet vs. Exercise in the Obesity Epidemic and The Role of Genes in the Obesity Epidemic.

There are eight more coming up. See the related posts below.

To date, about a hundred genetic markers have been linked to obesity, but when you put them all together, overall, they account for less than 3 percent of the difference in body mass index (BMI) between people. You may have heard about the “fat gene,” called FTO, short for FaT mass and Obesity-associated). It’s the gene most strongly linked to obesity, but it explains less than 1 percent of the difference in BMI between people, a mere 0.34 percent. 

As I discuss in my video The Role of Genes in the Obesity Epidemic, FTO codes for a brain protein that appears to affect our appetite. Are you one of the billion people who carry the FTO susceptibility genes? It doesn’t matter because it only appears to result in a difference in intake of a few hundred extra calories a year. The energy imbalance that led to the obesity epidemic is on the order of hundreds of calories a day, and that’s the gene known so far to have the most effect. The chances of accurately predicting obesity risk based on FTO status is “only slightly better than tossing a coin.” In other words, no, those genes don’t make you look fat.

When it comes to obesity, the power of our genes is nothing compared to the power of our fork. Even the small influence the FTO gene does have appears to be weaker among those who are physically active and may be abolished completely in those eating healthier diets. FTO only appears to affect those eating diets higher in saturated fat, which is predominantly found in meat, dairy, and junk food. Those eating more healthfully appear to be at no greater risk of weight gain, even if they inherited the “fat gene” from both of their parents.

Physiologically, FTO gene status does not appear to affect our ability to lose weight. Psychologically, knowing we’re at increased genetic risk for obesity may motivate some people to eat and live more healthfully, but it may cause others to fatalistically throw their hands up in the air and resign themselves to thinking that it just runs in their family, as you can see in the graph below and at 2:11 in my video. Obesity does tend to run in families, but so do lousy diets. 

Comparing the weight of biological versus adopted children can help tease out the contributions of lifestyles versus genetics. Children growing up with two overweight biological parents were found to be 27 percent more likely to be overweight themselves, whereas adopted children placed in a home with two overweight parents were 21 percent more likely to be overweight. So, genetics do play a role, but this suggests that it’s more the children’s environment than their DNA.

One of the most dramatic examples of the power of diet over DNA comes from the Pima Indians of Arizona. As you can see in the graph below and at 3:05 in my video, they not only have among the highest rates of obesity, but they also have the highest rates of diabetes in the world. This has been ascribed to their relatively fuel-efficient genetic makeup. Their propensity to store calories may have served them well in times of scarcity when they were living off of corn, beans, and squash, but when the area became “settled,” their source of water, the Gila River, was diverted upstream. Those who survived the ensuing famine had to abandon their traditional diet to live off of government food programs and chronic disease rates skyrocketed. Same genes, but different diet, different result. 

In fact, a natural experiment was set up. The Pima living over the border in Mexico come from the same genetic pool but were able to maintain more of their traditional lifestyle, sticking with their main staples of beans, wheat flour tortillas, and potatoes. Same genes, but seven times less obesity and about four times less diabetes. You can see those graphs below and at 3:58 and 4:02 in my video. Genes may load the gun, but diet pulls the trigger.

Of course, it’s not our genes! Our genes didn’t suddenly change 40 years ago. At the same time, though, in a certain sense, it could be thought of as all in our genes. That’s the topic of my next video The Thrifty Gene Theory: Survival of the Fattest.

This is the second in an 11-video series on the obesity epidemic. If you missed the first one, check out The Role of Diet vs. Exercise in the Obesity Epidemic. 

Obesity isn’t new, but the obesity epidemic is. We went from a few corpulent kings and queens, like Henry VIII or Louis VI (known as Louis le Gros, or “Louis the Fat”), to a pandemic of obesity, now considered to be “arguably the gravest and most poorly controlled public health threat of our time.” As you can see below and at 0:34 in my video The Role of Diet vs. Exercise in the Obesity Epidemic, about 37 percent of American men are obese and 41 percent of American women, with no end in sight. Earlier reports had suggested that the rise in obesity was at least slowing down, but even that doesn’t appear to be the case. Similarly, we had thought we were turning the corner on childhood obesity “[a]fter 35 years of unremittingly bad news,” but the bad news continues. Childhood and adolescent obesity rates have continued to rise, now into the fourth decade. 

Over the last century, obesity appears to have jumped ten-fold, from about 1 in 30 to now 1 in 3, but it wasn’t a steady rise. As you can see in the graph below and at 1:15 in my video, something seems to have happened around the late 1970s—and not just in the United States, but around the globe. The obesity pandemic took off at about the same time in the 1970s and 1980s in most high-income countries. The fact that the rapid rise “seemed to begin almost concurrently” across the industrialized world suggests a common cause. What might that trigger have been? 

Any potential driver would have to be global and “coincide with the upswing of the epidemic.” So, the change would have had to have started about 40 years ago and would have had to have been able to spread rapidly around the globe. Let’s see how all the various theories stack up. For example, as you can see below and at 1:55 in my video, some have blamed changes in our built environment and shifts in city planning that have made our communities less conducive to walking, biking, and grocery shopping. That doesn’t meet our criteria for a credible cause, though, because there was no universal, simultaneous change in our neighborhoods within that time frame.

When researchers surveyed hundreds of policymakers, most blamed the obesity epidemic on a “lack of personal motivation.” Do you see how little sense that makes? In the United States, for example, obesity shot up across the entire population in the late 1970s, as you can see at 2:26 in my video. I concur with the researchers who “believe it is implausible that each age, sex, and ethnic group, with massive differences in life experience and attitudes, had a simultaneous decline in willpower related to healthy nutrition or exercise.” More plausible than a global change like our characters would be some global change like our lives. 

The food industry blames inactivity. “If all consumers exercised,” said the CEO of PepsiCo, “obesity wouldn’t exist.” Coca-Cola went a step further, spending $1.5 million to create the Global Energy Balance Network to downplay the role of diet. Leaked emails show the company planned on using the front to “serve as a ‘weapon’ to ‘change the conversation’ about obesity in its ‘war’ with public health.

This tactic is so common among food and beverage companies that it even has a name: “leanwashing.” You’ve heard of greenwashing, where companies deceptively pretend to be environmentally friendly. Leanwashing is the term used to describe companies that try to position themselves as helping to solve the obesity crisis when they’re instead directly contributing to it. For example, the largest food company in the world, Nestlé, has “rebranded itself as the ‘world’s leading nutrition, health and wellness company.” Yes, that Nestlé, makers of Nesquik, Cookie Crisp, and historically more than a hundred different brands of candy, including Butterfinger, Kit Kat, Goobers, Gobstoppers, Runts, and Nerds. Another one of its slogans is “Good Food, Good Life.” Its Raisinets may have some fruit, but Nestlé seems to me more Willy Wonka than wellness. 

The constant corporate drumbeat of overemphasis on physical inactivity appears to be working. In response to the Harris poll question, “Which of these do you think are the major reasons why obesity has increased?,” a “huge majority of 83% chose lack of exercise, while only 34% chose excessive calorie consumption.” “Confusion about the effect of exercise on the energy balance” has been identified as one of the most common misconceptions about obesity. The scientific community has “come to a fairly decisive conclusion” that the factors governing calorie intake more powerfully affect overall calorie balance. It’s our fast food more than our slow motion. 

“There is considerable debate in the literature today about whether physical activity has any role whatsoever in the epidemic of obesity that has swept the globe since the 1980s.” The increase in caloric intake per person is more than enough to explain the obesity epidemic in the United States and also explain it globally. If anything, the level of physical activity over the last few decades has gone up slightly in both Europe and North America. Ironically, this may be a result of the extra energy it takes to move around our heavier bodies, making it a consequence of the obesity problem rather than the cause.

“Formal exercise plays a very small role in the total daily physical activity energy expenditure.” Think how much more physical work people used to do in the workplace, on the farm, or even in the home. It’s not just the shift in collar color from blue to white. Increasing automation, computerization, mechanization, motorization, and urbanization have all contributed to increasingly more sedentary lifestyles over the last century—and that’s the problem with the theory. The occupational shifts and advent of labor-saving devices “have been gradual and largely predated the dramatic increase in weight gain across the developed world in the past few decades.” Washing machines, vacuum cleaners, and the Model T were all invented before 1910. Indeed, when put to the test using state-of-the-art methods to measure energy in and energy out, it was caloric intake, not physical activity, that predicted weight gain over time. 

The common misconception that obesity is mostly due to lack of exercise may not just be a benign fallacy. Personal theories of causation appear to impact people’s weight. Those who blame insufficient exercise are significantly more likely to be overweight than those who implicate a poor diet. Put those who believe lack of exercise causes obesity in a room with chocolate, and they can covertly be observed consuming more candy. Those holding that view may be different in other ways, though. You can’t prove cause and effect until you put it to the test. And, indeed, as you can see in the graph below, and at 7:22 in my video, people randomized to read an article implicating inactivity went on to eat significantly more sweets than those reading about research that indicated diet. A similar study found that those presented with research blaming genetics subsequently ate significantly more cookies. The title of that paper? “An Unintended Way in Which the Fat Gene Might Make You Fat.” 

When I sat down to write How Not to Diet, I knew this “what triggered the obesity epidemic” was going to be a big question I had to face. Was it inactivity (just kids sitting around playing video games or scrolling on their phones)? Was it genetic? Was it epigenetic (something turning on our fat genes)? Or was it just the food? Were we eating more fat all of a sudden? More carbs? More processed foods? Or were we just eating more period, because of bigger serving sizes or more snacking? Inquiring minds wanted to know. 

This is the first in an 11-video series to answer this question, which I originally released in a two-hour webinar in 2020. Check out the webinar digital download here. Or, check them out in the related posts below.  

Instead of looking only at individual studies or individual reviews of studies, what if you looked at a review of reviews? In my last video, I covered beverages. As you can see below and at 0:20 in my video Friday Favorites: What Are the Best Foods?, the majority of reviews found some effects either way, finding at least some benefits to tea, coffee, wine, and milk, but not for sweetened beverages, such as soda. As I explored in depth, this approach isn’t perfect. It doesn’t take into account such issues as conflicts of interest and industry funding of studies, but it can offer an interesting bird’s-eye view of what’s out in the medical literature. So, what did the data show for food groups? 

You’ll note the first thing the authors did was divide everything into plant-based foods or animal-based foods. For the broadest takeaway, we can look at the totals. The vast majority of reviews on whole plant foods show protective or, at the very least, neutral effects, whereas most reviews of animal-based foods identified deleterious health effects or, at best, neutral effects, as you can see at 1:14 in my video. 

Let’s break these down. As you can see in the graph below and at 1:23, the plant foods consistently rate uniformly well, reflecting the total, but the animal foods vary considerably. If it weren’t for dairy and fish, the total for animal foods would swing almost entirely neutral or negative. 

I talked about the effects of funding by the dairy industry in my last blog, as well as substitution effects. For instance, those who drink milk may be less likely to drink soda, a beverage even more universally condemned than dairy, so the protective effects may be relative. They may arise not necessarily from what is being consumed, but rather from what is being avoided. This may best explain the fish findings. After all, the prototypical choice is between chicken and fish, not chicken and chickpeas.

Not a single review found a single protective effect of poultry consumption. Even the soda industry could come up with 14 percent protective effects! But, despite all of the funding from the National Chicken Council and the American Egg Board, chicken, and eggs got big fat goose eggs, as you can see below and at 2:20 in my video. 

Also, like the calcium in dairy, there are healthful components of fish, such as the long-chain omega-3 fatty acids. Not for heart health, though. In “the most extensive systematic assessment of effects of omega-3 fats on cardiovascular health to date,” increasing intake of fish oil fats had little or no effect on cardiovascular health. If anything, it was the plant-based omega-3s found in flaxseeds and walnuts that were protective. The long-chain omega-3s are important for brain health. Thankfully, just like there are best-of-both-worlds non-dairy sources of calcium, there are pollutant-free sources of the long-chain omega-3s, EPA, and DHA, as well.

The bottom line, as you can see below and at 3:04 in my video, is that when it comes to diet-related diseases, such as obesity, type 2 diabetes, mental health, bone health, cardiovascular disease, and cancers, even if you lump together all the animal foods, ignore any industry-funding effects, and just take the existing body of evidence at face value, nine out of ten study compilations show that whole plant foods are, in the very least, not bad.

However, about eight out of ten of the reviews on animal products show them to be not good, as shown in the graph below and at 3:24 in my video.

This reminds me of my Flashback Friday: What Are the Healthiest Foods? video, which you may find to be helpful for some broad takeaways.

If you missed my previous video, check out Friday Favorites: What Are the Best Beverages?.

The omega-3s video I mentioned is Should Vegans Take DHA to Preserve Brain Function?.

For more on eggs, see here.

On fish, go here.

And, for poultry, see related posts below. 

If you’ve watched my videos or read my books, you’ve heard me say, time and again, the best available balance of evidence. What does that mean? When making decisions as life-or-death important as what to feed ourselves and our families, it matters less what a single study says, but rather what the totality of peer-reviewed science has to say.

Individual studies can lead to headlines like “Study Finds No Link Between Secondhand Smoke and Cancer,” but to know if there is a link between secondhand smoke and lung cancer, it would be better to look at a review or meta-analysis that compiles multiple studies. The problem is that some reviews say one thing—for instance, “breathing other people’s tobacco smoke is a cause of lung cancer”—and other reviews say another—such as, the effects of secondhand smoke are insignificant and further such talk may “foster irrational fears.” And, while we’re at it, you can indulge in “active smoking of some 4-5 cigarettes per day” without really worrying about it, so light up!

Why do review articles on the health effects of secondhand smoke reach such different conclusions? As you can imagine, about 90 percent of reviews written by researchers affiliated with the tobacco industry said it was not harmful, whereas you get the opposite number with independent reviews, as you can see below and at 1:18 in my video Friday Favorites: What Are the Best Beverages?. Reviews written by the tobacco industry–affiliated researchers had 88 times the odds of concluding that secondhand smoke was harmless. It was all part of “a deliberate strategy to use scientific consultants to discredit the science…” In other words, “the strategic and long run antidote to the passive smoking issue…is developing and widely publicizing clear-cut, credible, medical evidence that passive smoking [secondhand smoke] is not harmful to the non-smoker’s health.”

Can’t we just stick to the independent reviews? The problem is that industry-funded researchers have all sorts of sneaky ways to get out of declaring conflicts of interest, so it can be hard to follow the money. For instance, it was found that “77% failed to disclose the sources of funding” for their research. But, even without knowing who funded what, the majority of reviews still concluded that secondhand smoke was harmful. So, just as a single study may not be as helpful as looking at a compilation of studies on a topic, a single review may not be as useful as a compilation of reviews. In that case, looking at a review of reviews can give us a better sense of where the best available balance of evidence may lie. When it comes to secondhand smoke, it’s probably best not to inhale, as you can see in the graph below and at 2:30 in my video. 

Wouldn’t it be cool if there were reviews of reviews for different foods and drinks? Voila! Enter “Associations Between Food and Beverage Groups and Major Diet-Related Chronic Diseases: An Exhaustive Review of Pooled/Meta-Analyses and Systematic Reviews.” Let’s start with the drinks. As you can see below and at 2:51 in my video, the findings were classified into three categories: protective, neutral, or deleterious.

First up: tea versus coffee. As you can see in the graph below and at 2:58, most reviews found both beverages to be protective for whichever condition they were studying, but you can see how this supports my recommendation for tea over coffee. Every cup of coffee is a lost opportunity to drink a cup of green tea, which is even healthier. 

It’s no surprise that soda sinks to the bottom, as you can see below and at 3:20 in my video, but 14 percent of reviews mentioned the protective effects of drinking soda. What?! Well, most were references to papers like “High Intake of Added Sugar Among Norwegian Children and Adolescents,” a cross-sectional study that found that eighth-grade girls who drank more soda were thinner than girls who drank less. Okay, but that was just a snapshot in time. What do you think is more likely? That the heavier girls were heavier because they drank less soda, or that they drank less sugary soda because they were heavier? Soda abstention may therefore be a consequence of obesity, rather than a cause, yet it gets marked down as having a protective association. 

Study design flaws may also account for wine numbers, as seen below and at 4:07 in my video. This review of reviews was published in 2014, before the revolution in our understanding of “alcohol’s evaporating health benefits,” suggesting that the “presumed health benefits from ‘moderate’ alcohol use [may have] finally collapsed”—thanks in part to a systematic error of misclassifying former drinkers as if they were lifelong abstainers, as I revealed in a deep dive in a video series on the subject.  

Sometimes there are unexplainable associations. For example, one of the soft drink studies found that increased soda consumption was associated with a lower risk of certain types of esophageal cancers. Don’t tell me. Was the study funded by Coca-Cola? Indeed. Does that help explain the positive milk studies, as you can see in the graph below and at 5:02 in my video? Were they all just funded by the National Dairy Council? 

As shown below and at 5:06, even more conflicts of interest have been found among milk studies than soda studies, with industry-funded studies of all such beverages “approximately four to eight times more likely to be favorable to the financial interests of the [study] sponsors than articles without industry-related funding.”

Funding bias aside, though, there could be legitimate reasons for the protective effects associated with milk consumption. After all, those who drink more milk may drink less soda, which is even worse, so they may come out ahead. It may be more than just relative benefits, though. The soda-cancer link seems a little tenuous and not just because of the study’s financial connection to The Coca-Cola Company. It’s hard to imagine a biologically plausible mechanism, whereas even something as universally condemned as tobacco isn’t universally bad. As I’ve explored before, more than 50 studies have consistently found a protective association between nicotine and Parkinson’s disease. Even secondhand smoke may be protective. Of course, you’d still want to avoid it. Passive secondhand smoke may decrease the risk of Parkinson’s, but it increases the risk of stroke, an even deadlier brain disease, not to mention lung cancer and heart disease, which has killed off millions of Americans since the first Surgeon General’s report was released, as you can see below and at 6:20 in my video. 

Thankfully, by eating certain vegetables, we may be able to get some of the benefits without the risks, and the same may be true of dairy. As I’ve described before, the consumption of milk is associated with an increased risk of prostate cancer, leading to recommendations suggesting that men may want to cut down or minimize their intake, but milk consumption is also associated with decreased colorectal cancer risk. This appears to be a calcium effect. Thankfully, we may be able to get the best of both worlds by eating high-calcium plant foods, such as greens and beans.  

What does our review-of-reviews study conclude about such plant-based foods, in comparison to animal-based foods? We’ll find out next.

Stay tuned for the exhaustive review of meta-analyses and systematic reviews on major diet-related chronic diseases found for food groups in What Are the Best Foods?.

The alcohol video I mentioned is Is It Better to Drink a Little Alcohol Than None at All?, and the Parkinson’s video is Pepper’s and Parkinson’s: The Benefits of Smoking Without the Risks. I also mentioned my Dairy and Cancer video. 

What about diet soda? See related posts below. 

What’s so bad about alcohol? Check out Can Alcohol Cause Cancer? and Do Any Benefits of Alcohol Outweigh the Risks? for more. 

I’ve also got tons of milk. Check here.

My recommendations for the best beverages are water, green tea, and hibiscus herbal tea. Learn more in the related posts below.

Headaches are one of the top five reasons people end up in emergency rooms and one of the leading reasons people see their doctors in general. One way to try to prevent them is to identify their triggers and avoid them. Common triggers for migraines include stress, smoking, hunger, sleep issues, certain foods (like chocolate, cheese, and alcohol), your menstrual cycle, or certain weather patterns (like high humidity).

In terms of dietary treatments, the so-called Father of Modern Medicine, William Osler suggested trying a “strict vegetable diet.” After all, the nerve inflammation associated with migraines “may be reduced by a vegan diet as many plant foods are high in anti-inflammatory compounds and antioxidants, and likewise, meat products have been reported to have inflammatory properties.” It wasn’t put to the test, though, for another 117 years.

As I discuss in my video Friday Favorites: Foods That Help Headache and Migraine Relief, among study participants given a placebo supplement, half said they got better, while the other half said they didn’t. But, when put on a strictly plant-based diet, they did much better, experiencing a significant drop in the severity of their pain, as you can see in the graph below and at 1:08 in my video. 

Now, “it is possible that the pain-reducing effects of the vegan diet may be, at least in part, due to weight reduction.” The study participants lost about nine more pounds when they were on the plant-based diet for a month, as shown below, and at 1:22. 

Even just lowering the fat content of the diet may help. Those placed on a month of consuming less than 30 daily grams of fat (for instance, less than two tablespoons of oil all day), experienced “statistically significant decreases in headache frequency, intensity, duration, and medication intake”—a six-fold decrease in the frequency and intensity, as you can see below and at 1:44 in my video. They went from three migraine attacks every two weeks down to just one a month. And, by “low fat,” the researchers didn’t mean SnackWell’s; they meant more fruits, vegetables, and beans. Before the food industry co-opted and corrupted the term, eating “low fat” meant eating an apple, for example, not Kellogg’s Apple Jacks.  

Now, they were on a low-fat diet—about 10 percent fat for someone eating 2,500 calories a day. What about just less than 20 percent fat compared to a more normal diet that’s still relatively lower fat than average? As you can see below and at 2:22 in my video, the researchers saw the same significant drops in headache frequency and severity, including a five-fold drop in attacks of severe pain. Since the intervention involved at least a halving of intake of saturated fat, which is mostly found in meat, dairy, and junk, the researchers concluded that reduced consumption of saturated fat may help control migraine attacks—but it isn’t necessarily something they’re getting less of. There are compounds “present in Live green real veggies” that might bind to a migraine-triggering peptide known as calcitonin gene-related peptide, CGRP. 

Drug companies have been trying to come up with something that binds to CGRP, but the drugs have failed to be effective. They’re also toxic, which is a problem we don’t have with cabbage, as you can see below and at 3:01 in my video. 

Green vegetables also have magnesium. Found throughout the food supply but most concentrated in green leafy vegetables, beans, nuts, seeds, and whole grains, magnesium is the central atom to chlorophyll, as shown below and at 3:15. So, you can see how much magnesium foods have in the produce aisle by the intensity of their green color. Although magnesium supplements do not appear to decrease migraine severity, they may reduce the number of attacks you get in the first place. You can ask your doctor about starting 600 mg of magnesium dicitrate every day, but note that magnesium supplements can cause adverse effects, such as diarrhea, so I recommend getting it the way nature intended—in the form of real food, not supplements.  

Any foods that may be particularly helpful? You may recall that I’ve talked about ground ginger. What about caffeine? Indeed, combining caffeine with over-the-counter painkillers, like Tylenol, aspirin, or ibuprofen, may boost their efficacy, at doses of about 130 mg for tension-type headaches and 100 mg for migraines. That’s about what you might expect to get in three cups of tea, as you can see below, and at 4:00 in my video. (I believe it is just a coincidence that the principal investigator of this study was named Lipton.) 

Please note that you can overdo it. If you take kids and teens with headaches who were drinking 1.5 liters of cola a day and cut the soda, you can cure 90 percent of them. However, this may be a cola effect rather than a caffeine effect. 

And, finally, one plant food that may not be the best idea is the Carolina Reaper, the hottest chili pepper in the world. It’s so mind-numbingly hot it can clamp off the arteries in your brain, as seen below and at 4:41 in my video, and you can end up with a “thunderclap headache,” like the 34-year-old man who ate the world’s hottest pepper and ended up in the emergency room. Why am I not surprised it was a man? 

I’ve previously covered ginger and topical lavender for migraines. Saffron may help relieve PMS symptoms, including headaches. A more exotic way a plant-based diet can prevent headaches is by helping to keep tapeworms out of your brain.

Though hot peppers can indeed trigger headaches, they may also be used to treat them. Check out my video on relieving cluster headaches with hot sauce. 

The American Medical Association started warning people about excess sugar consumption more than 75 years ago, based in part on our understanding that “sugar supplies nothing in nutrition but calories, and the vitamins provided by other foods are sapped by sugar to liberate these calories.” So, added sugars aren’t just empty calories, but negative nutrition. “Thus, the more added sugars one consumes, the more nutritionally depleted one may become.”

Given the “totality of publicly available scientific evidence,” the Food and Drug Administration (FDA) decided to make processed food manufacturers declare “added sugars” on their nutrition labels. The National Yogurt Association was livid and said it “continues to oppose the ‘added sugars’ declaration,” since it needed “‘added sugars’ to increase palatability” of its products. The junk food association questioned the science, whereas the ice cream folks seemed to imply that consumers are too stupid to “understand or know how to use the added sugar declaration,” so it’s better just to leave it off. The world’s biggest cereal company, Kellogg’s, took a similar tact, opposing it so as not “to confuse consumers.” Should the FDA proceed with such labeling against Kellogg’s objections, the cereal giant pressed that “an added sugars declaration…should be communicated as a footnote.” It claimed that its “goal is to provide consumers with useful information so they can make informed choices.” This is from a company that describes its Froot Loops as “packed with delicious fruity taste, fruity aroma, and bright colors.” Keep in mind that Froot Loops has more sugar than a Krispy Kreme doughnut, as you can see in the graph below and at 1:46 in my video Friday Favorites: Kids’ Breakfast Cereals as Nutritional Façade. 

Froot Loops is more than 40 percent sugar by weight! You can see the cereal box’s Nutrition Facts label below and at 1:50 in my video. 

The tobacco industry used similar terms, such as “light,” “low,” and “mild” to make its products appear healthier—before it was barred from doing so. “Now sugar interests are fighting similar battles over whether their terminology, including ‘healthy,’ ‘natural,’ ‘naturally sweetened,’ and even ‘lightly sweetened,’ is deceptive to consumers.”

But if you look at the side of a cereal box, as shown below and at 2:13 in my video, you can see all those vitamins and minerals that have been added. That was one of the ways the cereal companies responded to calls for banning sugary cereals. General Mills defended the likes of Franken Berry, Trix, and Lucky Charms for being fortified with essential vitamins. 

Sir Grapefellow, I learned, was a “grape-flavored oat cereal” complete with “sweet grape star bits”—that is, marshmallows. Don’t worry. It was “vitamin charged!” You can see that cereal box below and at 2:31 in my video. 

Sugary breakfast cereals, said Dr. Jean Mayer from Harvard, “are not a complete food even if fortified with eight or 10 vitamins.” Senator McGovern replied, “I think your point is well taken that these products may be mislabeled or more correctly called candy vitamins than cereals.” 

Plastering nutrient claims on cereal boxes can create “a ‘nutritional façade’ around a product, acting to distract attention away” from unsavory qualities, such as excess sugar content. Researchers found that the “majority of parents misinterpreted the meaning of claims commonly used on children’s cereals,” raising significant public health concerns. Ironically, cereal boxes bearing low-calorie claims were found to have more calories on average than those without such a claim. The cereal doth protest too much. 

Even candy bar companies are getting in on the action, bragging about protein content because of some peanuts. Like the Baby Ruth, a candy bar that has 50 grams of sugar. Froot Loops could be considered breakfast candy, as the same serving would have 40 sugar grams, as you can see below and at 3:45 in my video. 

Given that “research suggests that consumers believe front-of-package claims, perceive them to be government-endorsed, and use them to ignore the Nutrition Facts Panel,” there’s been a call from nutrition professionals to consider “an outright ban on all front-of-package claims.” The industry’s short-lived “Smart Choices” label, as you can see below and at 4:13 in my video, was met with disbelief when it was found adorning qualifying cereals like Froot Loops and Cookie Crisp. The processed food industry spent more than a billion dollars lobbying against the adoption of more informative labeling (a traffic-light approach), “opposing most aggressively the use of a red light suggesting that any food was too high in anything.” 

I was invited to testify as an expert witness in a case against sugary cereal companies. (I donated my fee, of course.) Check out the related posts below for a video series and blogs that are a result of some of the research I did. 

You may also be interested in videos and blogs on the food industry; see related posts below.

In my video on flexitarians, I discuss how the benefits of eating a plant-based diet are not all-or-nothing. “Simple advice to increase the consumption of plant-derived foods with compensatory [parallel] reductions in the consumption of foods from animal sources confers a survival advantage”— a live-longer advantage. The researchers call it a “pro-vegetarian” eating pattern, one that’s moving in the direction of vegetarianism, “a more gradual and gentle approach.” 

If you’re dealing with a serious disease, though, like diabetes, completely “avoiding some problem foods is easier than attempting to moderate their intake. Clinicians would never tell an alcoholic to try to simply cut down on alcohol. Avoiding alcohol entirely is more effective and, in fact, easier for a problem drinker…Paradoxically, asking patients to make a large change may be more effective than making a slow transition. Diet studies show that recommending more significant changes increases the chances that patients can accomplish [them]. It may help to replace the common advice, ‘all things in moderation’ with ‘big changes beget big results.’ Success breeds success. After a few days or weeks of major dietary changes, patients are likely to see improvements in weight and blood glucose [sugar] levels—improvements that reinforce the dietary changes that elicited them. Furthermore, they may enjoy other health benefits of a plant-based diet” that may give them further motivation. 

As you can see below and at 1:43 in my video Friday Favorites: Is Vegan Food Always Healthy?, those who choose to eat plant-based for their health say it’s mostly for “general wellness or general disease prevention” or to improve their energy levels or immune function, for example. 

They felt it gives them a sense of control over their health, helps them feel better emotionally, improves their overall health, makes them feel better, and more, as shown below and at 1:48. Most felt it was very important for maintaining their health and well-being. 

For the minority who used it for a specific health problem, mostly high cholesterol or weight loss, followed by high blood pressure and diabetes, most reported they felt it helped a great deal, as you can see below and at 2:14. 

Some choose plant-based diets for other reasons, such as animal welfare or global warming, and it looks like “ethical vegans” are more likely to eat sugary and fatty foods, like vegan donuts, compared to those eating plant-based because of religious or health concerns, as you can see below and at 2:26 in my video. 

The veganest vegan could make an egg- and dairy-free cake, covered with frosting, marshmallow fluff, and chocolate syrup, topped with Oreos, and served with a side of Doritos. Or, they may want fruit for dessert, but in the form of Pop-Tarts and Krispy Kreme pies. Vegan, yes. Healthy, no. 

“Plant-based diets have been recommended to reduce the risk of type 2 diabetes (T2D). However, not all plant foods are necessarily beneficial.” In the pro-vegetarian scoring system I mentioned above, you get points for eating potato chips and French fries because they are technically plant-based, as you can see below and at 3:07 in my video, but Harvard researchers wanted to examine the association of not only an overall plant-based diet, but healthy and unhealthy versions. So, they created the same kind of pro-vegetarian scoring system, but it was weighted towards any sort of plant-based foods and against animal foods; then, they created a healthful plant-based diet index, where at least some whole plant foods took precedence and Coca-Cola and other sweetened beverages were no longer considered plants. Lastly, they created an unhealthful plant-based diet index by assigning positive scores to processed plant-based junk and negative scores for healthier plant foods and animal foods. 

Their findings? As you can see below and at 3:51 in my video, a more plant-based diet, in general, was good for reducing diabetes risk, but eating especially healthy plant-based foods did better, nearly cutting risk in half, while those eating more unhealthy plant foods did worse, as shown in the graph below and at 4:03.

Now, is that because they were also eating more animal foods? People often eat burgers with their fries, so the researchers separated the effects of healthy plant foods, less healthy plant foods, and animal foods on diabetes risk. And, they found that healthy plant foods were protectively associated, animal foods were detrimentally associated, and less healthy plant foods were more neutral when it came to diabetes risk. Below and at 4:32 in my video, you can see the graph that shows higher diabetes risk with more and more animal foods, no protection whatsoever with junky plant foods, and lower and lower diabetes risk associated with more and more healthy whole plant foods in the diet. So, they concluded that, yes, “plant-based diets…are associated with substantially lower risk of developing T2D.” However, it may not be enough to just lower the intake of animal foods; consumption of less healthy plant foods may need to decrease, too. 

As a physician, labels like vegetarian and vegan just tell me what you don’t eat, but there are a lot of unhealthy vegetarian fare like French fries, potato chips, and soda pop. That’s why I prefer the term whole food and plant-based nutrition. That tells me what you do eat—a diet centered around the healthiest foods out there. 

The video I mentioned is Do Flexitarians Live Longer?. 

You may also be interested in some of my past popular videos and blogs on plant-based diets. Check related posts below. 

Dating back to the original “Dietary Goals for the United States” in 1977, also known as the so-called McGovern Report, leading nutrition scientists didn’t only call for a reduction in meat and other sources of saturated fat and cholesterol, such as dairy and eggs, but also sugar. The goal was to reduce America’s sugar intake to no more than 10 percent of our daily diet.

“The conclusions would hang sugar,” reported the president of the Sugar Association. “The McGovern Report has to be neutralized.” The National Cattlemen’s Association was on its side and, just like Big Sugar, appealed to the Senate Select Committee to withdraw the report.

“The Sugar Industry Empire Strikes Back”—and it appeared to work. When the official U.S. Dietary Guidelines were released in 1980 and again in 1985, it was without a specific limit, like 10 percent. It “said, simply, and in just four words, ‘Avoid too much sugar.’” (Whatever that means.) “In 1990, it went to five words, ‘Use sugars only in moderation,’ and in 1995 to six: ‘Choose a diet moderate in sugars.’” In 2000, it at least went back to limiting intake—specifically, “‘Choose beverages and foods to limit your intake of sugars’ (ten words), but even that was too strong. Under pressure from sugar lobbyists, the government agencies substituted the word ‘moderate’ for ‘limit’ so it read ‘Choose beverages and foods to moderate your intake of sugars.’” Then, the 2005 guidelines committee dropped the s-word completely, encouraging Americans to “Choose carbohydrates wisely…” Again, what does that mean? If only there were a dietary guidelines committee that could guide us….

The Sugar Association expressed optimism about that 2005 Committee. In its Sugar E-News, it wrote that Sugar Association Incorporated (SAI) “is committed to the protection and promotion of sucrose [table sugar] consumption. Any disparagement of sugar will be met with forceful, strategic public comments”—and it wasn’t kidding. “In 2003, [the World Health Organization] WHO released a joint report with the Food and Agriculture Organization entitled Diet, nutrition and the prevention of chronic diseases which, for the first time [since the McGovern Report], called for a reduction in sugar intake to under 10% of total dietary energy [caloric] consumption.” The Sugar Association responded by threatening to get the United States to withdraw all funding from the WHO. You can see it yourself in black and white at 2:22 in my video Friday Favorites: The Recommended Daily Added Sugar Intake. The Sugar Association threatened to pressure Congress to withdraw funding from the World Health Organization—polio vaccinations and AIDS medications be damned! Don’t mess with the candy man. The threat was described as “tantamount to blackmail and worse than any pressure exerted by the tobacco lobby.” 

Fifteen years later and 40 years after the first proposed McGovern Report, the 2015 to 2020 Dietary Guidelines for Americans lays out the 10 percent limit as a key recommendation: “Consume less than 10 percent of calories per day from added sugars.” This is currently exceeded by every age bracket in the United States starting at age one, as you can see in the graph below and at 2:58 in my video, with adolescents averaging 87 grams of sugar a day. That means the average teen is effectively eating 29 sugar packets a day. 

The Sugar Association describes the 10 percent limit as “extremely low.” Well, I mean, it is only up to about a dozen spoonsful a day. Of course, there is no dietary requirement for added sugar at all, and every single calorie we get from added sugar is a wasted opportunity to get calories from sources that provide nutrition. To the American Heart Association’s credit, it went further by trying to push added sugar intake down to about 6 percent of calories, for which a single can of soda could send you over the limit. That’s an added sugar limit exceeded by 90 percent of Americans.

In 2017, the American Heart Association (AHA) released its guidelines for children, recommending they get no more than about six teaspoons per day. In that case, a single serving of nearly a hundred cereals on the U.S. market would exceed the entire recommended daily limit. The AHA recommends no added sugars at all for children under the age of two, a recommendation that’s violated in up to 80 percent of toddlers, as you can see below and at 4:20 in my video. 

In the United States, “at least 65 countries have implemented dietary guidelines or public health policies to curb sugar consumption to encourage maintenance of healthy body weight.” In the United Kingdom, the Scientific Advisory Committee on Nutrition made new recommendations to reduce added sugars down to 5 percent, which is also the direction the World Health Organization is headed. The WHO always seems to be ahead of the curve. Why? Because its policy-making process is at least partially protected “against industry influence.” Unlike governments, which may have competing interests in commerce and trade, “WHO is exclusively concerned with health.”

I spoke at a hearing of the 2020 Dietary Guidelines Committee. Watch the highlights and my speech here: Highlights from the 2020 Dietary Guidelines Hearing.

The sugar industry keeps pretty busy, as you’ll see from my recent videos, Friday Favorites: Are Fortified Kids’ Breakfast Cereals Healthy or Just Candy? and Flashback Friday: Sugar Industry Attempts to Manipulate the Science.

Check the related posts below for my other popular videos and blogs on sugar.

Please tell us a little bit about your work and career.
My name is Sheil Shukla, DO, and I am a board-certified internal medicine physician with Northwestern Medicine in Illinois. I am the creator behind @plantbasedartist on Instagram and the author of the vegan cookbook Plant-Based India (published August 2022), which was named one of The New York Times Best Cookbooks of 2022 and nominated for a 2023 James Beard Foundation Book Award. 

As a doctor, what do you envision as the way forward to encourage people to include more fruits and vegetables into their diets?
As a primary care physician, I believe one way forward to encouraging more consumption of fruits and vegetables is to educate the medical community about the merits of a plant-based diet. When patients hear this information from their physicians and other medical providers, I think many can be receptive to it. I think it is more important now than ever to combat the misinformation on diets and nutrition that pervades social and traditional media.

What key message would you like to share with our audience about nutrition and public health?
Nutrition plays an incredibly powerful role in public health. Beyond increasing awareness of the benefits of a plant-based diet, I believe more resources should be directed toward the widespread access to healthful foods and addressing food deserts. Furthermore, I look forward to the day that medical providers are equally equipped to counsel their patients regarding nutrition as they do pharmacotherapy. 

What are some plant-based ingredients and vegan dishes you would like to highlight as traditional to your culture?
The vast array of spices and legumes is most definitely a highlight of Indian culture. These ingredients are not only incredibly nutrient-dense, but they form the backbone of plant-based Indian cuisine. Some of my favorite spices include cumin, coriander, fennel, and turmeric, and some of my favorite legumes include mung beans, black chickpeas, and red lentils––all of which are used widely throughout Indian cuisine.

What does AAPI Month mean to you, and how is it significant to the work you do?
AAPI Month draws attention to the incredibly diverse and vibrant AAPI community. For me, it means learning from those around me and sharing more about my culture and heritage with others. We are all the better when we share and grow together.

Please tell us a little bit about your book, Plant-Based India. Plant-Based India documents my culinary heritage—the recipes and techniques that have been passed down in my family for generations. It highlights plant-forward aspects of Indian cuisine, in a way that is accessible to the western kitchen and pantry. My cookbook includes more than 100 hearty Indian and Indian-inspired recipes that I developed and photographed myself.

Gājjar No Halvo Baked Oatmeal

Ingredients

• 1 cup (100 g) old-fashioned rolled oats
• 2 tablespoons ground flax seeds
• 1 tablespoon chia seeds
• 1½ teaspoons ground cinnamon
• ½ teaspoon ground ginger
• ½ teaspoon ground cardamom
• Pinch of grated nutmeg
• 1½ cups (360 ml) unsweetened soy milk or other nondairy milk
• 2 ripe bananas, mashed (about ¾ cup/180 g)
• 2 carrots, grated (about ¾ cup/75 g)
• 5 Medjool dates, finely chopped (about ½ cup/75 g)
• 1 teaspoon vanilla extract or vanilla bean paste
• ⅓ cup (40 g) chopped raw nuts, such as almonds, pistachios, or walnuts
• Unsweetened soy milk, warmed
• Pinch of ground cinnamon

Instructions

1. Preheat the oven to 350°F (175°C).
2. Mix together the oats, flax, chia, cinnamon, ginger, cardamom, and nutmeg in a large bowl until well combined.
3. Add the soy milk, bananas, carrots, dates, vanilla, and half of the chopped nuts, and mix until thoroughly combined.
4. Transfer the mixture to an 8 to 9-inch (20 to 23 cm) round, square, or oval baking dish. Sprinkle with the remaining nuts and bake until the oats and carrots are tender, about 30 minutes.
5. Serve warm with a bit of warmed soy milk and a pinch of ground cinnamon. Keep leftovers in the refrigerator for a few days and reheat with more milk as needed.

Recipe from Plant-Based India: Nourishing Recipes Rooted in Tradition © Dr. Sheil Shukla, 2022. Reprinted by permission of The Experiment. Available everywhere books are sold. theexperimentpublishing.com

For more from Dr. Shukla, check out www.sheilshukla.com and @plantbasedartist on Instagram.

It’s been recognized for decades that cigarette smoking can have “a major effect” on bone health, “increasing the lifetime risk of hip fracture by about half.” It also appears to impair bone healing, so much so that surgeons ask if they should discriminate against smokers because their bone and wound-healing complication rates are so high. What about smoking marijuana?

As I discuss in my video Effects of Marijuana on Weight Gain and Bone Density, “There is accumulating evidence to suggest that cannabinoids [cannabis compounds] and their receptors play important roles in bone metabolism by regulating bone mass, bone loss, and bone cell function.” Okay, but are they “friend or foe?” 

“Results from research on cannabinoids and bone mineral density in rodent models have been inconsistent. Some studies show increased bone formation, others have demonstrated accelerated bone loss, and yet others have shown no association. This variation in results may be due [in part] to differences in the mouse strain, sex, age…” If you can’t even extrapolate from one mouse to another, how can you extrapolate from mice to human beings?

What if you just measure cannabis use and bone mineral density in people? Researchers tested thousands of adults and asked them about their cannabis use. There did not appear to be any link between the two, which is a relief. However, in this study, “heavy” cannabis use was defined as just five or more days of use in the previous 30 days. The researchers didn’t ask beyond that, so, theoretically, someone who smoked just five joints in their entire life could be categorized as a “heavy user” if they happened to use it five times in the last four weeks.

How about cannabis use on 5,000 separate occasions over a lifetime? Now that’s a heavy user—decades of regular use. In that case, heavy use was “associated with low bone mineral density and an increased risk of fractures”—about double the fracture rate presumably due to lower bone density in the hip and spine, although heavy cannabis users were also thinner on average, and thinner people have lighter bones.

Hip fracture risk goes down as our weight goes up. Nearly half of underweight women have osteoporosis, but less than 1 percent of obese women do, which makes total sense. Being obese forces our body to make our bones stronger to carry around all of that extra weight. That’s why weight-bearing exercise is so important to constantly put stress on our skeleton. When it comes to our bones, it’s use it or lose it. That’s why astronauts can lose a percent of their bone mass every month in “long-duration spaceflight.” Their bodies aren’t stupid. Why waste all that energy making a strong skeleton if you aren’t going to put any weight on it? 

So, maybe the reason heavy cannabis users have frailer bones is because they tend to be about 15 pounds lighter. Wait a second. Marijuana users are slimmer? What about the munchies? “The lower BMI that was observed in heavy cannabis users at first sight seems counterintuitive,” given marijuana’s appetite stimulation, but this isn’t the first time this has been noted. 

“Popular culture commonly depicts marijuana users as a sluggish, lethargic, and unproductive subculture of compulsive snackers,” and marijuana has indeed been found to increase food intake. A single hit can increase appetite, so you’d expect obesity rates to rise in states that legalized it. But, if anything, the rise in obesity appeared to slow after medical marijuana laws were passed, whereas it appeared to just keep rising in other states, as you can see in the graph below and at 3:45 in my video. 

The reason pot smokers may be slimmer is because of the effect of smoked marijuana on metabolism. We’ve known for more than nearly 40 years that within 15 minutes of lighting up, our metabolic rate goes up by about 25 percent and stays there for at least an hour, as you can see below and at 4:04 in my video. So, that may be playing a role. 

Is that why heavy cannabis use is associated with lower bone mineral density and increased risk of fractures? Because users just aren’t as overweight? No. Even when taking BMI into account, heavy cannabis use appears to be “an independent predictor” of weaker bones.

I originally released a series of marijuana videos in a webinar and downloadable digital DVD. There are still a few videos coming out over the next year, but if you missed any of the already published ones, see the related posts below. 

For more on bone health, check out the related posts below. 

There’s a condition known as seasonal affective disorder that is characterized by increased appetite and cravings, as well as greater sleepiness and lethargy, that begins in autumn when light exposure starts to dwindle. This now appears to represent the far end of a normal spectrum of human behavior. We appear to eat more as the days get shorter. There is a “marked seasonal rhythm” to calorie intake with greater meal size, eating rate, hunger, and overall calorie intake in the fall. 

In preparation for winter, some animals hibernate, doubling their fat stores with autumnal abundance to deal with the subsequent scarcity of winter. Genes have been identified in humans that are similar to hibernation genes, which may help explain why we exhibit some of the same behaviors, and the autumn effect isn’t subtle. As you can see in the graph below and at 1:06 in my video Friday Favorites: Why People Gain Weight in the Fall, researchers calculated a 222-calorie difference between how many calories we consume in the fall versus the spring. This isn’t just because it’s colder, either, since we eat more in the fall than in the winter. It appears we’re just genetically programmed to prep for the deprivation of winter that no longer comes. 

It’s remarkable that, in this day and age of modern lighting and heating, our bodies would still pick up enough environmental cues of the changing seasons to have such a major influence on our eating patterns. Unsurprisingly, bright light therapy is used to treat seasonal affective disorder, nearly tripling the likelihood of remission, compared to placebo. Though it’s never been tested directly, it can’t hurt to take the dog out for some extra morning and daytime walks in the fall to try to fend off some of the coming holiday season weight gain.

People blame the holidays for overeating, but it may be that “rather than the holidays causing heightened intake, the seasonal heightening of intake in the fall may have caused the scheduling of holidays at that time.”

Regardless, as you can see below and at 2:15 in my video, other “specific recommendations for the prevention of obesity and metabolic syndrome by improving the circadian system health,” based on varying degrees of evidence, include: sleeping during the night and being active during the day; sleeping enough—at least seven or eight hours a night; early to bed, early to rise; and short naps are fine. (Contrary to popular belief, daytime napping does not appear to adversely impact sleep at night.) Also recommended: avoiding bright light exposure at night; sleeping in total darkness when possible; making breakfast or lunch your biggest meal of the day; not eating or exercising right before bed; and completely avoiding eating at night. 

This was the last video in my chronobiology series. If you missed any of the others, check out the related posts below.

If weakening our circadian rhythm can cause weight gain, might strengthening it facilitate weight loss? You may remember the child’s swing analogy I shared previously. Regular morning meals can give our cycles a little daily push, but the biggest shove comes from our exposure to bright morning light. Similarly, exposure to light at night could be analogous to nighttime eating, as you can see below and at 0:31 in my video Shedding Light on Shedding Weight.

Of course, we’ve had candles to illuminate our nights for 5,000 years, but flames from candles, campfires, and oil lamps are “strongly skewed towards the red end of the [light] spectrum; as a result, firelight has much less impact on circadian rhythmicity than electric light.” It’s the shorter blue wavelengths that specially set our circadian clocks. Electric lighting, which we’ve only had for a little over a century, “has gradually changed since the 1960s from an incandescent-bulb form consisting of mainly low-level yellow wavelengths to high-intensity discharge forms,” such as fluorescents and LED lights, “that contain blue wavelengths,” which are more similar to morning sunlight and have the strongest effect on our circadian rhythm.

Using wrist meters to measure ambient light exposure, researchers found that increased exposure to light in the evening and nighttime correlated with a subsequent increased risk of developing obesity over time. This was presumed to be due to circadian misalignment, but might it instead be a sign of not sleeping as much, and maybe that’s the real reason people grew heavier? This was controlled for in a study of more than 100,000 women, which found that the odds of obesity trended with higher nighttime light exposure independent of sleep duration.

Compared to women who reported their bedrooms at night were either too dark to see their hand in front of their face or at least dark enough that they couldn’t see across the room, those who reported their bedrooms were light enough to see across the room were significantly heavier. They weren’t all sleeping with nightlights on either. Without blackout curtains on windows, many neighborhoods may be bright enough to cause circadian disruption. Using satellite imagery, scientists have even been able to correlate higher obesity rates with brighter communities. There’s so much light at night these days that, outside of a blackout, the only Milky Way our children will likely ever see is inside a candy wrapper.

Although sleep quantity could be controlled, what about sleep quality? Maybe people sleeping in bedrooms that aren’t as dim don’t sleep as soundly, leaving them too tired to exercise the next day, for example. You can’t know for sure if nocturnal light exposure is harmful in and of itself until you put it to the test. When that was done, those randomized to exposure to bright light for a few hours in the evenings or exposed even just for a single night suffered adverse metabolic consequences. 

The more intriguing question then becomes: Can circadian syncing with morning bright light therapy be a viable weight-loss strategy? Insufficient morning light may be the circadian equivalent of skipping breakfast. Indoor lighting is too bright at night, but it may be too dim during the day to robustly boost our daily rhythm. Light exposure from getting outdoors in the morning, even on an overcast day, is correlated to lower body weight compared to typical office lighting, so some doctors started trying “phototherapy” to treat obesity. The first case reports began being published in the 1990s. Three out of four women lost an average of about four pounds over six weeks of morning bright light exposure, but there was no control group to confirm the effect. 

Ten years later, the first randomized controlled trial was published. Overweight individuals were randomized to an exercise intervention with or without an hour a day of bright morning light. Compared to normal indoor lighting, the bright light group lost more body fat, but it’s possible the light just stimulated them to exercise harder. Studies show that exposure to bright light, even the day prior to exercise, may boost performance. In a handgrip endurance test, exposure to hours of bright light increased the number of contractions until exhaustion from about 770 to 860 the next day. While light-induced improvements in activity or mood can be helpful in their own right, it would be years later still before we finally learned whether the light exposure itself could boost weight loss. 

Following an unpublished study in Norway purporting to show a dozen-pound weight-loss advantage to eight weeks of 30 minutes of daily daylight (compared to indoor lighting), researchers tried three weeks of 45 minutes of morning bright light compared to the same time sitting in front of an “ion generator” that appeared to turn on but was secretly deactivated. As you can see in the graph below and at 5:08 in my video, the three weeks of light beat out the placebo, but the average difference in body fat reduction was only about a pound. This slight edge didn’t seem to correlate with mood changes, but bright light alone can stimulate serotonin production in the human brain and cause the release of adrenaline-type hormones, both of which could benefit body fat aside from any circadian effects. 

Regardless of the mechanism, bright morning daylight exposure could present a novel weight-loss strategy straight out of the clear blue sky.  

I have a whole series on chronobiology. You can see all of the videos on the topic page. The last few are listed below in the related posts and help to paint the full picture of how our environment can affect our circadian rhythms.

For more on weight loss, you can also check out my recent series in the related posts below, or browse all of my weight loss videos here. 

What Is a Heart Stent?

You may have heard of open-heart surgery, performed to try to bypass the blockage, or percutaneous coronary intervention. As discussed in my video Why Angioplasty Heart Stents Don’t Work Better, historically, the more common procedure was angioplasty, wherein a tiny balloon is inserted into a narrowed coronary artery feeding your heart to force it to open wider to improve blood flow. Then, stents came into vogue. Instead of just ballooning up the artery, how about permanently inserting a metal mesh tube to prop open the artery? Stents are typically inserted in the groin and threaded all the way up into the heart, and, while stents used to be mostly bare metal, there are now fancy new drug-eluting stents that not only force open arteries, but they also slowly release pharmaceuticals.

How Serious Is Having a Stent Put In?

The surgical procedure carries risks—including death. In an emergency setting, while you’re actively having a heart attack, angioplasty can be lifesaving, but hundreds of thousands of these procedures are for stable coronary artery disease, for which there appears to be little or no benefits. As discussed in my video The Risks of Heart Stents, doctors appear to be killing or stroking out thousands of people a year for nothing, and that isn’t even counting the tens of thousands of silent mini-strokes caused by these procedures that may contribute to cognitive decline. Indeed, 11 to 17 percent of people who go through angioplasty or stenting come away with new brain lesions—up to one in six patients.

Do Stents Work?

Angioplasty and stents for non-emergency coronary artery disease are among the most common invasive procedures performed in the United States. Millions of people have gotten stents for stable coronary artery disease, yet it now appears that for such patients, angioplasty and stent placement do not actually prevent heart attacks, do not offer long-term angina pain relief, and do not improve survival. Why? Because the most dangerous plaques—the ones most vulnerable to rupture leading to a heart attack—are not the ones doctors put stents into. They often aren’t the ones that are even seen on angiogram to be obstructing blood flow.

Indeed, in 2007, we learned from the COURAGE trial that angioplasty and stents don’t reduce the risk of death or heart attack, but patients didn’t seem to get the memo. As discussed in my video Why Are Stents Still Used If They Don’t Work?, only 1 percent realize there was no mortality or heart attack benefit, perhaps because most cardiologists failed to happen to mention that fact. One can imagine that if patients actually understood all they were getting was symptomatic relief, they’d be less likely to go under the knife. Ten years later, the ORBITA trial was published, showing even the promise of symptom relief was an illusion.

Are Stents Really Necessary?

The implications are profound and far-reaching. First and foremost, the results showed unequivocally that there are no benefits to non-emergency angioplasty and stents for stable heart disease. Basically, patients would be risking harm for no benefit whatsoever, so it’s hard to imagine a scenario where a fully-informed patient would choose an invasive procedure for nothing.

Yet angioplasty and stent placement continue to be frequently performed for patients with non-emergency coronary artery disease, despite clear evidence that it provides minimal benefit, as discussed in my video Angioplasty Heart Stent Risks vs. Benefits. For example, it does not prevent heart attacks or death, yet as many as nine out of ten patients mistakenly believed that the procedure would reduce their chances of having a heart attack.

What Are the Side Effects of Heart Stents?

Stent placement and the blood-thinner drugs you have to go on after the surgery can cause complications, including heart failure, stroke, and death. The risks are relatively low; there’s less than a 1 percent chance it will kill you or stroke you out. The 15 percent risk of heart attack is only if your stent clogs at a later date, which only happens about 1 percent of the time in the near-term. There is a 13 percent risk of kidney injury, due to the dyes that must be injected, but that typically heals on its own. The most serious complications—including death—only happen in about 1 in 150 cases. However, you have to multiply that by the fact that hundreds of thousands of these procedures are performed every year.

And, again, although stents appeared to offer immediate relief of angina chest pain in stable patients with coronary artery disease, they do not offer long-term angina pain relief and they didn’t actually translate into lower risk of heart attack or death. More on this in my video Do Heart Stent Procedures Work for Angina Chest Pain?.

Diet After Heart Attack and Stents

Should we be surprised that angioplasty and stents fail to improve prognosis? After all, neither does anything to modify the underlying disease process itself. In other words, they don’t treat the cause. As discussed in my video Heart Stents and Upcoding: How Cardiologists Game the System, even if stents helped with symptoms beyond the placebo effect, they would still just be treating the symptoms, not the disease, so it’s no wonder the disease continues to progress until the patient is disabled into death.

Thankfully, we are on the cusp of a seismic revolution in health: not another pill, procedure, or operation, but, instead, treating the underlying cause of heart disease with whole food, plant-based nutrition, the mightiest tool medicine has ever had in its toolbox.

Heart-Healthy Eating

The most likely reason the majority of our loved ones will die is heart disease. Atherosclerosis, or hardening of the arteries, begins in childhood, as discussed in my video How Not to Die from Heart Disease. The arteries of nearly all kids raised on the standard American diet already have fatty streaks marking the first stage of the disease—by the time they are ten years old. After that, the plaques start forming in our 20s, get worse in our 30s, and can then start killing us off. In our heart, it’s called a heart attack; in our brain, it can manifest as a stroke. So, for anyone reading this who is older than ten, the choice isn’t whether or not to eat healthfully to prevent heart disease—it’s whether or not you want to reverse the heart disease you likely already have.

Is that even possible? When researchers took people with heart disease and put them on the kind of plant-based diet followed by populations who did not get epidemic heart disease, their hope was that it might slow down the disease process or maybe even stop it. Instead, something miraculous happened. The disease actually started to reverse. It started to get better. As soon as patients stopped eating artery-clogging diets, their bodies were able to start dissolving away some of the plaque, opening up arteries without drugs and without surgery, suggesting their bodies wanted to heal all along, but just were never given the chance. That improvement in blood flow to the heart muscle itself was after just three weeks of eating healthfully.

Plant-based diets aren’t just safer and cheaper. They can work better because they let us treat the actual cause of the disease.

Shift workers may have higher rates of death from heart disease, stroke, diabetes, dementia, and cardiovascular disease, as well as higher rates of death from cancer. Graveyard shift, indeed! But, is it just because they’re eating out of vending machines or not getting enough sleep? Highly controlled studies have recently attempted to tease out these other factors by putting people on the same diets with the same sleep—but at the wrong time of day. Redistributing eating to the nighttime resulted in elevated cholesterol and increases in blood pressure and inflammation. No wonder shift workers are at higher risk. Shifting meals to the night in a simulated night-shift protocol effectively turned about one-third of the subjects prediabetic in just ten days. Our bodies just weren’t designed to handle food at night, as I discuss in my video The Metabolic Harms of Night Shifts and Irregular Meals.

Just as avoiding bright light at night can prevent circadian misalignment, so can avoiding night eating. We may have no control over the lighting at our workplace, but we can try to minimize overnight food intake, which has been shown to help limit the negative metabolic consequences of shift work. When we finally do get home in the morning, though, we may disproportionately crave unhealthy foods. In one experiment, 81 percent of participants in a night-shift scenario chose high-fat foods, such as croissants, out of a breakfast buffet, compared to just 43 percent of the same subjects during a control period on a normal schedule.

Shiftwork may also leave people too fatigued to exercise. But, even at the same physical activity levels, chronodisruption can affect energy expenditure. Researchers found that we burn 12 to 16 percent fewer calories while sleeping during the daytime compared to nighttime. Just a single improperly-timed snack can affect how much fat we burn every day. Study subjects eating a specified snack at 10:00 am burned about 6 more grams of fat from their body than on the days they ate the same snack at 11:00 pm. That’s only about a pat and a half of butter’s worth of fat, but it was the identical snack, just given at a different time. The late snack group also suffered about a 9 percent bump in their LDL cholesterol within just two weeks.

Even just sleeping in on the weekends may mess up our metabolism. “Social jetlag is a measure of the discrepancy in sleep timing between our work days and free days.” From a circadian rhythm standpoint, if we go to bed late and sleep in on the weekends, it’s as if we flew a few time zones west on Friday evening, then flew back Monday morning. Travel-induced jet lag goes away in a few days, but what might the consequences be of constantly shifting our sleep schedule every week over our entire working career? Interventional studies have yet put it to the test, but population studies suggest that those who have at least an hour of social jet lag a week (which may describe more than two-thirds of people) have twice the odds of being overweight. 

If sleep regularity is important, what about meal regularity? “The importance of eating regularly was highlighted early by Hippocrates (460–377 BC) and later by Florence Nightingale,” but it wasn’t put to the test until the 21st century. A few population studies had suggested that those eating meals irregularly were at a metabolic disadvantage, but the first interventional studies weren’t published until 2004. Subjects were randomized to eat their regular diets divided into six regular eating occasions a day or three to nine daily occasions in an irregular manner. Researchers found that an irregular eating pattern can cause a drop in insulin sensitivity and a rise in cholesterol levels, as well as reduce the calorie burn immediately after meals in both lean and obese individuals. The study participants ended up eating more, though, on the irregular meals, so it’s difficult to disentangle the circadian effects. The fact that overweight individuals may overeat on an irregular pattern may be telling in and of itself, but it would be nice to see such a study repeated using identical diets to see if irregularity itself has metabolic effects.

Just such a study was published in 2016: During two periods, people were randomized to eat identical foods in a regular or irregular meal pattern. As you can see in the graph below and at 4:47 in my video, during the irregular period, people had impaired glucose tolerance, meaning higher blood sugar responses to the same food.

They also had lower diet-induced thermogenesis, meaning the burning of fewer calories to process each meal, as seen in the graph below and at 4:55 in my video.

The difference in thermogenesis only came out to be about ten calories per meal, though, and there was no difference in weight changes over the two-week periods. However, diet-induced thermogenesis can act as “a satiety signal.” The extra work put into processing a meal can help slake one’s appetite. And, indeed, “lower hunger and higher fullness ratings” during the regular meal period could potentially translate into better weight control over the long term. 

The series on chronobiology is winding down with just two videos left in this series: Shedding Light on Shedding Weight and Friday Favorites: Why People Gain Weight in the Fall.

If you missed any of the other videos, see the related posts below. 
 

The number one killer in the United States and around the world is what we eat. As you can see in the graph below and at 0:15 in my video Friday Favorites: Are Ancient Grains Healthier?, our diet kills millions more than tobacco. What are the five most important things we can do to improve our diets, based on the single most comprehensive global study of the health impact of nutrition? Eat less salt, eat more nuts, eat more non-starchy vegetables, eat more fruit, and, finally, eat more whole grains. 
Any particular type of whole grains? What about so-called ancient grains? Are they any better than modern varieties? For instance, what about kamut, described as “mummy wheat” and supposedly unearthed from an Egyptian tomb?

After WWII, the wheat industry selected particularly high-yielding varieties for pasta and bread. Over the past few years, though, some of the more ancient grains—“defined as those species that have remained unchanged over the last hundred years” despite agricultural revolutions—have been reintroduced to the market.

As you can see below and at 1:13 in my video, nutritionally, kamut and einkorn wheat, which is the oldest wheat, have more eyesight-improving yellow carotenoid pigments, such as lutein and zeaxanthin, compared to modern bread and pastry wheat, because the pigments have been bred out of the bread intentionally. People want their white bread white, but modern pasta flour (durum wheat) maintains much of that yellow nutritional hue. 

As you can see in the graph below and at 1:41 in my video, modern wheat may have less lutein, but it tends to have more vitamin E, as seen in the graph below and at 1:45. Based on straight vitamin and mineral concentrations, it’s pretty much a wash. Both modern and primitive kinds of wheat have a lot of each, but primitive wheats do have more antioxidant capacity, likely due to their greater polyphenol content, as you can see in the graph below and at 2:00 in my video. To know if that makes any difference, though, we have to put it to the test. 

If you expose human liver cells to digested bread made out of ancient grains (kamut and spelt), heritage kinds of wheat, or modern strains, then expose the cells to an inflammatory stimulus, the modern wheat strains seem less able to suppress the inflammation, as you can see in the graphs below and at 2:09 in my video. The investigators conclude that even though these different grains seem to be very similar nutritionally, they appear to exert different effects on human cells, “confirming the potential health benefits of ancient grains.” 
That was in a petri dish, though. What about people? If ancient kinds of wheat are better at suppressing inflammation, what if you took people with irritable bowel syndrome (IBS) and randomized them to receive six weeks of wheat products made out of modern wheat or ancient wheat—in this case, kamut? Same amount of wheat, just different types. If there is no difference between the wheats, there’d be no difference in people’s symptoms, right? But, when study participants in the control group were switched to the ancient wheat kamut, they experienced less abdominal pain, less frequent pain, less bloating, more satisfaction with stool consistency, and less interference with their quality of life, compared to the modern wheat. So, after switching to the ancient wheat, they had “a significant global improvement in the extent and severity of symptoms related to IBS…”

What about liver inflammation? The liver function of those with nonalcoholic fatty liver disease randomized to eat kamut improved, compared to those eating the same amount of regular wheat, suggesting kamut is superior, as you can see below and at 3:47 in my video.

People with diabetes, had better cholesterol and better insulin sensitivity on the same ancient grain, as shown below and at 3:57.

And those with heart disease? They had better blood sugar control and better cholesterol, as shown below and at 4:03. 

And, people without overt heart disease had better artery function, as you can see below and at 4:06 in my video.

The bottom line is that findings derived from human studies suggest that ancient wheat products are more anti-inflammatory and may improve things like blood sugar control and cholesterol. “Given that the overall number of human interventional trials conducted to date are numerically insufficient, it is not possible to definitively conclude that ancient wheat varieties are superior to all commercial, modern wheat counterparts in reducing chronic disease risk.” However, the best available data do suggest they’re better for us.  

Regardless of what type of wheat you may eat, a word to the wise: Don’t eat the plastic bread-bag clip. A 45-year-old man presented with bloody stools, and his CT scan showed the offending piece of plastic from his bag of bread, as you can see below and at 4:53 in my video. When the patient was questioned, he “admitted to habitually eating quickly without chewing properly.” 

Whole grains—ideally intact ones and ancient and modern varieties alike—are an integral part of my Daily Dozen checklist, the healthiest of healthy things I encourage everyone to try to fit into their daily routines.  

Whole grains are especially good for our microbiome. Learn more in the related posts below.  What about gluten? Also, see the related posts below. 

Our entire digestive tract is, too. The rate at which our stomach empties, the secretion of digestive enzymes, and the expression of transporters in our intestinal lining for absorbing sugar and fat all cycle around the clock. So, too, does the ability of our body fat to sop up extra calories. The way we know these cycles are driven by local clocks, rather than being controlled by our brain, is that you can take surgical biopsies of fat, put them in a petri dish, and watch them continue to rhythm away.

All of this clock talk is not just biological curiosity. Our health may depend on keeping all of them in sync. “Imagine a child playing on a swing.” Picture yourself pushing, but you become distracted by what’s going on around you in the playground and stop paying attention to the timing of the push. So, you forget to push or you push too early or too late. What happens? Out of sync, the swinging becomes erratic, slows, or even stops. That is what happens when we travel across multiple time zones or have to work the night shift.

The “pusher” in this case is the light cues falling onto our eyes. Our circadian rhythm is meant to get a “push” from bright light every morning at dawn, but if the sun rises at a different time or we’re exposed to bright light in the middle of the night, this can push our cycle out of sync and leave us feeling out of sorts. That’s an example of a mismatch between the external environment and our central clock. Problems can also arise from a misalignment between the central clock in our brain and all the other organ clocks throughout our body. An extreme illustration of this is a remarkable set of experiments suggesting that even our poop can get jet lag.

As you can see below and at 2:31 in my video How to Sync Your Central Circadian Clock to Your Peripheral Clocks, our microbiome seems to have its own circadian rhythm.

Even though the bacteria are down where the sun doesn’t shine, there’s a daily oscillation in both bacterial abundance and activity in our colon, as you can see in the graph below and at 2:43 in my video. Interesting, but who cares? We all should. 

Check this out: If you put people on a plane and fly them halfway around the world, then feed their poop to mice, those mice grow fatter than mice fed preflight feces. The researchers suggest the fattening flora was a consequence of “circadian misalignment.” Indeed, several lines of evidence now implicate “chronodisruption”—the state in which our central and peripheral clocks diverge out of sync—as playing a role in conditions such as premature aging and cancer, as well as ranging to others like mood disorders and obesity.

Exposure to bright light is the synchronizing swing pusher for our central clock. What drives our internal organ clocks that aren’t exposed to daylight? Food intake. That’s why the timing of our meals may be so important. Researchers removed all external timing cues by keeping study participants under constant dim light and found that you could effectively decouple central rhythms from peripheral ones just by shifting meal times. They took blood draws every hour and biopsies of the subjects’ fat every six hours to demonstrate the resulting metabolic disarray.

Just as morning light can help sync the central clock in our brain, morning meals can help sync our peripheral clocks throughout the rest of our body. Skipping breakfast disrupts the normal expression and rhythm of these clock genes themselves, which coincides with adverse metabolic effects. Thankfully, they can be reversed. Take a group of habitual breakfast-skippers and have them eat three meals at 8:00 am, 1:00 pm, and 6:00 pm, and their cholesterol and triglycerides improve, compared to taking meals five hours later at 1:00 pm, 6:00 pm, and 11:00 pm. There is a circadian rhythm to cholesterol synthesis in the body, too, which is also “strongly influenced by food intake.” This is evidenced by the 95 percent drop in cholesterol production in response to a single day of fasting. That’s why a shift in meal timing of just a few hours can result in a 20-point drop in LDL cholesterol, thanks to eating earlier meals, as you can see below and at 5:00 in my video. 

If light exposure and meal timing help keep everything synced, what happens when our circumstances prevent us from sticking to a normal daytime cycle? We’ll find out in The Metabolic Harms of Night Shifts and Irregular Meals. If you’re just coming into the series, be sure to check out the related posts below.  

The Evidence-Based Eating Guide

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Daily Dozen Meal Planning Guide

The healthiest diet is one that maximizes the intake of foods-as-grown—whole, plant-based foods—and minimizes the consumption of processed and animal-based foods. In the first half of his book, How Not to Die, Dr. Greger covers the whys of eating healthfully, exploring diet’s role in the prevention, treatment, and sometimes even reversal of the fifteen leading causes of death in the United States. In the book’s second half, he dives into the hows of eating healthfully and shares his Daily Dozen checklist, grocery shopping tips, and meal planning ideas.

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