The GMO Debate: A Case of False Dichotomies

by Hannah Packman

The use of genetic modification in our food system is a polarizing issue. However, the current discourse often ignores the grey areas, and may be detrimental to the public understanding of GMOs.

The ability and willingness to admit mistakes is often considered the typification of the wise and modest scientist. As science is an ever-evolving discipline, it is necessary for those within the field to adapt their thoughts and beliefs with emerging discoveries. Many are reluctant to concede their errors, as they worry it will threaten their scientific authority, but those who do are frequently lauded for their honesty and bravery in doing so. This phenomenon is generally observed in the context of divisive issues, such as climate change, antibiotic resistance, and carcinogenic chemicals.

Most recently, the use of GMOs has been the hot-button issue, not just within agro-ecology, but science as a whole. A number of researchers and journalists have publically “come out” on one side of the issue or the other.

Thierry Vrain, once a high-profile biotechnologist and genetic engineer, became an anti-GMO spokesperson upon retirement. He now warns of the dangers of genetically modified crops, urging that engineered soy and corn contain toxic and allergenic proteins. Vrain also questions the environmental justification of genetic modification; that these crops have higher yields and require less pesticides is unsubstantiated. Vrain is celebrated as a luminary by the anti-GMO camp, and is frequently quoted by organizations like GMWatch, Food Integrity Now, and Natural Society.

On the other side of the equation, Bill Nye, a previous GMO skeptic, recently came out in support of genetic modification after spending time with Monsanto’s scientists. The Washington Post, Business Insider, EcoWatch, and the Environmental Working Group all praised Nye’s conversion to a pro-GMO stance.

Admitting the error of one’s ways is certainly a courageous and admirable act. However, in situations such as these, perhaps an even bolder act is admitting ignorance. Given the contradictory evidence on the safety and effectiveness of GMOs, one would be remiss to conclusively choose either side.

True, GMOs hold great promise to solve our most pressing health, environmental, and economic concerns. For instance, genetically engineered crops can be manipulated to contain concentrated amounts of certain nutrients of concern in an effort to prevent deficiency-related disease. Golden rice, an engineered variety of rice with high levels of vitamin A, is the most obvious example. Vitamin A deficiency typically afflicts those in developing countries with limited access to food; annually, it causes blindness in as many as 500,000 children, and is responsible for 670,000 infant deaths. By providing necessary vitamin A, golden rice may be a valuable tool to promote ocular health and abate infant mortality.

Similarly, GMOs have significant potential to improve the environmental sustainability of agriculture by decreasing the use of land and chemicals.  Bt-corn is one of such engineered crops that have obviated the need for synthetic pesticides. This corn variety has been modified to express proteins from Bacillus thuringiensis, a bacterium that acts as a biopesticide. As such, Bt-corn is poisonous to pests, who are killed after ingesting the engineered crop. (Bt does not appear to have the same effect on humans, and the EPA says it can be ingested without deleterious consequences.)

Because this variety of corn acts as its own pesticide, the use of additional chemical pesticides is not always necessary. This could decrease exposure to and consumption of potentially toxic chemicals. According to a 2012 study at Washington State University, Bt crops have reduced pesticide use by 123 million pounds since 1996. It should be noted, however, that overall pesticide use increased by 404 million pounds, largely due to genetically engineered, herbicide resistant crops.

There are a number of other salient arguments in support of GM agriculture.  Certain engineered crops enable farmers to implement no-till methods, ultimately reducing soil erosion and, less directly, water pollution and eutrophication. GM crops may be a more economically reliable option for farmers, as they are less susceptible to the contingencies of weather, weeds, and insects. Furthermore, engineered crop varieties often have greater yield than their non-modified counterparts. The benefit of this is twofold: farmers will be guaranteed a greater payback for the same amount of land, while unsuitable land can be retired without threatening food supply.

Given the aforementioned benefits of genetic modification, it seems that opposing these wonder-crops would be an act of irrational skepticism. But for every argument in support of GMOs, there is an equally compelling argument against. For one, there is the concern of safety. Although GMO proponents maintain that modified crops are safe for human consumption, the research that supports this claim are typically short-term, experimental studies. The long-term effects of consuming genetically modified foods are unknown.

Of primary concern is allergenicity, as introducing allergenic protein sequences into a non-allergenic organism could possibly render the latter allergenic. Whether allergenicity is likely to occur in GM crops is a contested issue; many argue that the probability is no greater than in non-modified foods. Regardless, the causes of food allergies are still largely misunderstood, and the research on the safety of genetically engineered crops is relatively nascent, making it difficult to accurately assess the possibility of allergenicity.

Even if allergenicity is not a problem, there are other health risks associated with genetic modification.  As previously mentioned, herbicide-resistant GM crops have resulted in greater overall application of weed killers in the United States. Glyphosate (popularly known as Roundup), the most popular herbicide in the United States is, was recently identified by the World Health Organization as a likely carcinogen. Because a large portion of our food supply is treated with glyphosate, it is reasonable to ask about the ramifications of ingesting trace amounts on a daily basis.  In large quantities, it can be fatal.

The toxicity of herbicides is hazardous not just to humans, but to livestock and wildlife as well. Liberal herbicide application can affect all flora and fauna within an ecosystem, poisoning pollinators, and hindering the growth of plants that rely on them. In turn, the animals that use those plants as sustenance or habitat may also be threatened, causing a chain reaction that can shatter an entire ecosystem.

The possibility of pesticide resistance is of additional concern. As we introduce more Bt crops, the number of resistant species increases. There are now five pest species that exhibit resistance, and that number is expected to grow. The issue of herbicide resistance is even more prevalent; there are at least 30 weed species worldwide that exhibit glyphosate resistance. Pesticide and herbicide resistance is not a matter of inconvenience. As weeds and insects become resistant to chemicals, they evolve into “superweeds” and “superbugs,” extremely resilient species that, in large enough populations, will threaten our food supply.

The intent of presenting these arguments is not to sway you towards or away from GMOs; indeed, it is just the opposite. Genetic modification is an extraordinarily nuanced issue, and each application varies significantly in its benefits and its risks. By framing it as a black-and-white matter, one ignores the hundreds of gradations between. It is clear, then, that the question at hand is not “yes or no?” but rather “when?” “how?” and “why?” And in allowing for greater complexity in our discussion of GMOs, we will be more pragmatic in our future development and use of biotechnology.

Hannah Packman is a first year student in the Agriculture, Food and Environment masters program. When she isn’t busy filling her head with food-related facts, she enjoys filling her stomach with food-related objects.

Vitamin K2: What Is It, Where Is It, What Does It Do, and Do I Need It?

by Emily Finnan, RD

10 years ago, vitamin K2 was largely unheard of. Today, it’s a top Google search term, the subject of numerous books, and over 500 supplements are sold on Amazon. In part, due to a growing number of vitamin K2 supporters who champion it as a necessity for bone and heart health. However, 76 years after its discovery, it seems we still have more questions than answers about this important nutrient.

What is it?

Vitamin K2 isn’t a new nutrient; it’s simply a form of vitamin K. Vitamin K is a term for a group of essential

compounds that all contain the chemical structure methyl-1,4-napthoquinone.  This group can be further divided into vitamin K1, K2 and K3. Vitamin K2, or menaquinones, is a term for several compounds named MK-4 through MK-13.

Where is it?

Vitamin K2 is predominantly made by bacteria. It’s found in fermented foods and animal products.

MK-7 and MK-4 are the two most talked about and studied forms of vitamin K2. MK-7 is the form found in Natto, a Japanese fermented soy product. MK-4 is the form found in animal products. Additionally, your body likely makes MK-4 from vitamin K1 eaten. The other “MKs” are made by different strains of bacteria found in fermented foods or in your gastrointestinal tracts. It’s debated, but likely a minimal amount of vitamin K from the gut is actually absorbed and used by your body.

Vitamin K1, or phylloquinone, is made by plants. It’s found in a variety of vegetables, some fruits, and vegetable oils. Leafy greens are an especially good source. 90% of the vitamin K we eat is in this form.

Vitamin K3, or menadione, is a synthetic precursor of vitamin K. It isn’t recommend for humans, but it is used in animal feed.

What about grass-fed?

Blogs that tout the benefits of vitamin K2 likely recommend grass-fed animal products as the premier source. Grass does contain vitamin K1. But a cow’s primary source of vitamin K comes from large colonies of K2-producing bacteria that live in their ruminant stomachs. Conventionally raised livestock are frequently given antibiotics, which can diminish gut bacteria. However, livestock feed is typically fortified with vitamin K3, which the animal directly converts o MK-4.

MK-4 is present in conventionally-raised dairy, beef, poultry, and other animal-based foods. A study conducted in the Netherlands, found no substantial difference in MK-4 content between wild, free-range, and “intensively raised” meat, dairy, and eggs. Currently, there isn’t evidence to support grass-fed animals as a superior source of MK-4.

What does it do?

All forms of vitamin K help carboxylate (add extra acid groups) to certain proteins, which helps the proteins’ function. Un-carboxylated vitamin K-dependent proteins are those that vitamin K has not acted on.

Vitamin K & blood clotting

This is vitamin K’s most studied role. Vitamin K is essential for proper blood clotting. A person with a severe vitamin K deficiency, which is rare, will have clotting problems.

Vitamin K & bone

Vitamin K carboxylates the bone protein, osteocalcin, allowing it to act on bone. This has led to the hypothesis that a high level of un-carboxylated osteocalcin is an indicator of vitamin K insufficiency and poor bone health. Vitamin K2 and K1 have been shown to increase osteocalcin carboxylation. Additionally, researchers have found both inside bone.

Two large Japanese observational studies, totaling almost 3,000 people, found positive associations between dietary MK-7 and increased bone mineral density. However, observational trials can’t determine causation. People who eat more vitamin K, might have a healthier diet and lifestyle; especially because vitamin K is found in typically healthful foods.

Randomized controlled trials (RCT) can help determine causation. 11 RCTs have been conducted with 15 to 45 milligram (or 15,000 to 45,000 micrograms) MK-4 supplements. The majority do report that the MK-4 supplement group had a positive result in at least one marker of bone health.  In Japan, where most of these trials were conducted, MK-4 supplements are routinely used as part of osteoporosis treatment. Of note, these doses of vitamin K are much higher than you can obtain from food. Vitamin K is therefore being used as a medication, not as a dietary factor.

RCTs and observational trials conducted using vitamin K1 are inconclusive.

Vitamin K & vascular calcification

Vitamin K may have a role in preventing vascular calcification, a major risk factor for heart disease. This is through vitamin K’s carboxylation of matrix Gla-protein (MGP). It’s not fully understood, but un-carboxylated MGP may increase vascular calcification.  Vitamin K1 and MK-4 both reduce un-carboxylated MGP.

Only one observational, cohort study has shown a positive association between total dietary vitamin K2 intake and reduced vascular calcification. Observational studies using vitamin K1 intake show no effect.  An RCT, conducted at the Jean Mayer USDA Human Nutrition Research Center on Aging (HNRCA), found that vitamin K1 supplementation did slow progression of calcification in those with pre-existing coronary artery calcification.

Do I need it?

The optimum level of vitamin K in the diet is unclear. The adequate intake (AI) of vitamin K, for men 19 years and older, is 120 micrograms (mcg). This was based simply on the amount of vitamin K healthy people eat. The AI doesn’t specify targets of vitamin K1 versus K2. It’s been suggested that the amount of vitamin K needed to prevent clotting problems is less than 10 mcg per day; but at least 1,000 mcg per is needed for optimum bone density.

Below is a table of vitamin K content in various foods. The Vitamin K1 data is predominately from the USDA Nutrient Database. Vitamin K2 data was obtained from three individual studies: here, here, and here.


*unknown fat-content

Many books and health blogs (here, here, here, and here) claim that the US population is widely deficient  in vitamin K2, which they report is specifically essential for bone and vascular health. However, there is a lot more we need learn about vitamin K2. Do vitamin K2 and K1 actually have different functions in our body? If we can make vitamin K2 from K1, does it even matter how much K2 we eat? We don’t know what a sufficient level of vitamin K2 is, let alone a deficient level, or even the best biomarker of K2 status. Furthermore, if 1,000 mcg is the true optimum intake then it seems it would be much easier to reach this level by focusing on vitamin K1 sources rather than K2- you’d need to eat 7 pounds of blue cheese or 300 eggs a day to reach 1,000 mcg!

The good news is that a varied diet that includes variety of vegetables, leafy greens, as well as meats and dairy can supply a person with well over the AI of vitamin K. There is also no known harm of taking high-dose vitamin K supplements. My advice: eat a varied diet that includes servings of vitamin K-rich vegetables and fermented foods. These foods are great for other reasons too– high in other important micronutrients and fermented foods contain beneficial probiotics. If you’re thinking about taking a vitamin K2 supplement, talk to your doctor as vitamin K does interact with some medications.

Emily Finnan is a dietitian and finishing her first year in the Biochemical and Molecular Nutrition master’s program.  She’ll be getting acquainted with vitamin K this summer, completing a practicum in the HNRCA’s vitamin K laboratory.

Are Your Diet Choices Based in “Fact” or “Faith?” One Religion Professor Thinks It’s the Latter

by Katherine Pett

Looking for a nutritional antidote to food fears? Take a look at new release The Gluten Lie by Alan Levinovitz, PhD, and stop being scared of your sandwich.


Despite what the sinister cover of The Gluten Lie by Alan Levinovitz, PhD, suggests, this book is not about gluten… entirely. When I first picked it up, I assumed the author meant to proclaim that gluten sensitivity, the diagnosis du jour, is nonexistent. But the book makes little attempt to determine what is and isn’t healthy. In fact, it’s the exact opposite of a diet book.

A religion professor at James Madison University, Levinovitz remains agnostic about the existence of gluten sensitivity: to him, it may exist or may not. In fact, he takes this neutral tone with every food fad he discusses, from banishing sugar to forbidding fat. There is evidence for and against each recommendation, but not as much as you’d think.

Levinovitz is primarily concerned with the belief systems that cause sweeping dietary crazes. As a professor of religion, no one is more capable of delivering the Good Word: Many of our beliefs about food are more religious than rational in nature. We unconsciously base food choices and food fears on faith, not facts.

The strict-sounding title is based on the book’s thesis: If you tell people something is true when the research is inconclusive, it’s a lie. Unlike religious leaders for whom myths are tools to give hope and guidance to a congregation, people who invoke science—rather than God—to inspire behavior change have an obligation to the truth, the whole truth, and nothing but the truth.

In the book, Levinovitz uncovers which nutrition “facts” are more rooted in legend than reality and reveals the (sometimes sordid) history behind them. For each of these hotly-debated food elements (ex., gluten, fat, salt, and sugar), there are authorities who swear that eliminating it will fix your life.

For example, gluten restriction, especially as a part of the CrossFit/Paleo paradigm, can seem a little, well, cultish. But it’s nothing compared to the originators of sodium-restriction who formed an actual cult. Known as “Ricers,” these people were a group of extremist dieters who followed low-sodium, rice-diet guru Dr. Walter Kemper of Duke University. The Rice Diet was not unlike today’s Paleo or Bulletproof diets in that it attracted a lot of attention and plenty of celebrity adherents, such as Buddy Hacket, Dom DeLuise, and multiple NFL players. It was different, however, in the sense that its founder kept a harem of devoted dieting women in houses he owned, connected their housing via walkways, and was named an heir in their wills.

But why, you might be wondering, would people believe that a no-sodium, all-rice diet will solve your problems? Especially now when people have access to Google, PubMed, and a world of scientific references and textbooks that tell us that balance is key to health? It turns out that it isn’t hard to make a convincing and seemingly science-based argument. All you need to do is pick a few studies, conveniently tweak the details so they match your framework, add a few scary statistics and unproven claims and, boom, you’ve written the next Wheat Belly.

To prove his point, Levinovitz shows how it’s done with a diet of his own invention: The UNpacked DietTM. In the book’s last chapter, Levinovitz creates a mock first chapter of a “science-based” diet book that explains how plastic packaging will make you sick and fat. The diet comes complete with numerous citations, references to seemingly authoritative researchers, and excellent graphics tracking bottled water use and the rise in obesity. Even though I knew the diet was meant to be facetious, I found myself seriously considering some of the arguments. “That sounds reasonable,” I heard my inner-voice saying.

Just after he nearly convinced me that plastic really is the source of all my problems, Levinovitz then repeats the entire chapter, but with cartoon thought bubbles pointing out each flaw in the reasoning. Every single point that seemed so meaningful is actually a careful misrepresentation of evidence that doesn’t prove nearly as much as the “author” would like. The similarities between the writing in The UNpacked DietTM and any other diet book gracing the bestseller list are uncanny. In fact, it made me wonder if Dr. Levinovitz missed an opportunity by deciding to pull back the curtain on the genre, rather than to partake in its riches.

Overall take? If you work in wellness or you’re just an avid follower of nutrition in the news, you need this book. If you have an annoying friend who bugs you about the newest “antinutrient,” you need this book so you can toss it to your annoying friend while you run away. This book is timely, given the wake of The Food Babe, expands understanding of the belief systems that underlie our country’s disordered eating culture, and acts as a reset button for our own food prejudices.

While he may not make the point directly, it is implied throughout the book: You can’t cheat death with “one simple trick” to get rid of belly fat. There is no toxic nutrient that causes all disease. So chill out. Eat your sandwich.

Interested? Check out a recent lecture by Levinovitz, where he explains the concept of his book:

Katherine Pett is a first-year Biochemical and Molecular Nutrition student at The Friedman School.  Follow her on twitter @smarfdoc or contact her at 

The Yolk is Back in Town: Does Cholesterol Still Matter?

by Ally Gallop, BSc, RDN, CDE

Cherry picking through the Dietary Guidelines Advisory Committee’s (DGAC) February report is a nutrition communicator’s nightmare. Though the report is 571 pages deep, media headlines repeatedly echo the lack of a recommendation surrounding a seemingly new leniency towards cholesterol. This year, the DGAC points to inadequate evidence linking high dietary cholesterol to high serum cholesterol. So what changed? And why should we, as nutrition communicators, care?

The 2015 DGAC’s report recommends withdrawing cholesterol’s longstanding upper limit of 300 milligrams (mg) per day when updating the 2015 dietary guidelines set to occur later this year. Since the federal government’s dietary guidelines were first officially released in 1980, there has always been a focus on cholesterol and saturated fat. The initial guidelines stated to “avoid too much fat, saturated fat, and cholesterol.” It took until the fourth version in 1995 to place a hard number on cholesterol: 300 mg daily for the general population. A stricter 200 mg was advised for those with high cholesterol, at risk of cardiovascular disease (CVD), or diabetes. It also took until 1990 for specific limits on saturated fat to be made: less than 10% total caloric intake from saturated fat (the 2010 goal is now less than 7%).

So how did eggs become roped into this? In the 1950s, egg consumption averaged 374 per year or roughly a daily egg. With 186 mg cholesterol and 1.6 grams saturated fat per large egg, this dietary staple was a clear target. At the time, dietary cholesterol was thought to increase LDL (the “bad” cholesterol”) and one’s risk of CVD. Fast-forward to the 1990s and consumption plummeted to 236 (0.6 eggs per day). Even with this reduction, CVD remains the leading cause of death for both men and women. Marion Nestle relates this to poor communication with the public. Assumptions that Americans would adopt these dietary restrictions by replacing butter, beef, and cheese “with healthy fruits and vegetables… was naïve.” Americans were eating more refined carbohydrates, sugar, and sweeteners, items known to contribute to excess body weight, increased LDL, type 2 diabetes, and CVD risk.

Yet as far back as the 1990’s, experts began to learn that eating cholesterol does not necessarily parallel large increases in one’s risk of CVD. In 1999, the Journal of the American Medical Association found that despite an egg’s cholesterol, daily consumption did not increase one’s risk. Harvard’s School of Public Health’s Walter Willett has voiced how although this recommendation was initially based on well-intentioned theory, it stuck around due to inertia. The restriction was based on and supported by short-term studies with no consistent, hard, and direct evidence

So too, agreed the joint American Heart Association-American College of Cardiology task force in 2013 when it reported that cholesterol’s initial strict limit was based on studies too broad to find a direct link. Even so, the United States remains the only country to include a cholesterol limit within its dietary guidelines.

Adding to the complexity, cholesterol is produced by the liver having multiple roles throughout the body. It’s necessary for the production of steroid hormones, is present within the membrane of every cell, and is a requirement for fat absorption due to its role as a precursor for bile acids. In fact, the liver produces upwards of 85% of the body’s total cholesterol levels. Additionally, Willett shares how “It has become clear that eggs raise both LDL and HDL [the “good” cholesterol], so the impact on heart disease is less clear, and of course eggs contain much more than cholesterol.” And so they do. Eggs improve our:

  • Eyes: due to the antioxidants lutein and zeaxanthin, which help prevent macular degeneration
  • Brain: dietary choline is hard to come by, so eggs are a unique source
  • Muscles: there’s a reason why this high quality protein is rampant in a weight lifter’s diet
  • Satiety: the protein keeps us feeling full for longer, thereby being a useful addition to weight loss and maintenance eating patterns

But guess what? Your dietary advice hasn’t really changed.

The implications surrounding food communicators involve the public’s perception that nutritionists are forever changing their minds as to what’s healthy and what’s not. But taken together with saturated fat, the recommendations don’t really change.

The USDA and the Department of Health and Human Services will be responsible for updating the forthcoming dietary guidelines. If they adopt the DGAC’s recommendations, no longer having a guideline does not mean that foods containing cholesterol should be consumed without restraint. The vehicle that cholesterol is carried in still matters. As mentioned, cholesterol tends to coincide with saturated fat and exists primarily in animal foods, to which the DGAC continues to recommend restricting to no more than 7% of all calories. For instance, items with both high cholesterol and saturated fat include cheese and other high-fat dairy products; pizza; and many cuts of beef, pork, and poultry (with the skin).

In defense of the DGAC, Tufts own Dr. Alice Lichtenstein reports how the average American now consumes between 250 and 350 mg daily. Among other pertinent dietary factors, focusing on cholesterol is no longer of dire concern for the DGAC. However, although dietary cholesterol may not be of concern to the committee, saturated fat still is.

Rather than focusing on specific nutrients, its not enough for food communicators to solely depend on moderation and the importance of whole foods and diets when counseling patients. From experience, they want specific answers. So here’s what you need to know:

  • In 2012 3% of Americans had diabetes, another 86 million were in the prediabetic state, and 1.7 million new cases were diagnosed. In total, 85.6 million Americans suffer from CVD or the aftermath of stroke. Acknowledging that the dietary guidelines are intended for the general population, with numbers this large nutrition communicators need to avoid making broad strokes when advising the public.
  • A daily egg is fine, except for those with diabetes* who should limit their intake to no more than three yolks per week.
  • For those with or at risk for CVD and/or diabetes, continue with a 200 mg restriction.
  • Remain conservative with foods high in saturated fat. For instance, avoid 3-egg omelets with a side of bacon and sausage.
  • Opt for high-fiber foods and whole grains, since refined carbohydrates can lower HDL (nay) and fiber can help lower LDL (yay!).
  • For those pregnant or immune-compromised, cook eggs fully.

Remember that as of 2012 9.3% of Americans had diabetes, another 1.7 million new cases were diagnosed, and 86 million were in the prediabetic state. In total, 85.6 million Americans suffer from CVD or the aftermath of stroke. Acknowledging that the dietary guidelines are intended for the general public as a preventative health measure, with numbers this large nutrition communicators need to avoid making broad strokes when advising the public.

And ultimately, Dr. Lichtenstein reminds us how “all bets are off as to what the 2015 [dietary guidelines] will be.” Only time will tell if the 300 mg restriction lives on.

Want to have input on the 2015 dietary guidelines? The public comment period was recently extended until May 8, 2015. Click here to have your voice heard.

Ally Gallop, BSc, RD, CDE is studying towards an MS/MPH focusing in nutrition communication and behavior change. Her favorite egg dish is a scrambled egg, avocado, black beans, sweet potatoes, and Sriracha sauce.

To Juice, to Soup, or to Just Eat

by Emily Finnan, RD, LDN

Gwyneth Paltrow, Dr. Oz, and future bachelorette Kaitlyn Bristowe are a few embracing the latest weight loss and health solution: souping. Yes, move over juicing—souping is what’s hot.

The Soup CleansePea Soup

A soup cleanse doesn’t mean alternating between minestrone and clam chowder for a week. The soups are akin to smoothie, made of blended fruits and vegetables. Soupure, kitskitchen, and Real Food Works are a few companies offering soup cleanses. Some soups are served hot, others cold. There’s a romaine lettuce and tomatillo soup, strawberry sprouted cashew soup, and one of the few animal based soups: curried chicken.

The premise is simple. For one to five days, you eat only the soup shipped to you.  For about $60 a day you’ll get between four and six soups. Some companies offer additional flavored water and broths as part of their cleanse package.

The Juice Cleanse

Souping and juicing are the same concept. In juicing, for one to five days you drink only water or tea and five to six fruit and/or vegetable juice blends. Pressed Juicery and Suja offer juice cleanses between $55 and $72 a day.  Joe Cross, the star of Fat, Sick, and Nearly Dead, is the founder of Reboot with Joe. This company provides free recipe plans for a juice cleanse; accompanied by juicer and personal coaching marketing.

Health Claims

Souping and juicing boast similar health claims; including, detoxing from said built-up toxins, weight loss, energy boost, rest for your gastrointestinal tract, and a host of other claims. Some cleanse diets also instruct people to undergo periods of fasting or laxative use.

Studies on juicing or souping are limited. In one German study, participants drank 150-300 Calories of juice per day for about a week. They found some favorable changes in blood fat levels.  However, a week later, all levels were back to where they’d started. This speaks to the fact that any type of diet, followed only in the short-term, will have likely have little overall impact. This applies to weight loss claims too. A person could potentially lose weight on these low-Calorie cleanses, but if they switch back to their high-Calorie habitual diet, the weight will surely return.

This 2010 Sprout article examined the controversy surrounding detox diets. The “detoxing” concept, to put it plainly, doesn’t make sense. Juices and soups do not eliminate toxic compounds from the body. The only things that can do this are your liver, kidneys, intestines, and lungs. Life-long healthy habits, including a good diet, are important to keep these organs in good shape.

Soup and juice cleanse makers do not – as they should – recommend following their diets long-term. Doing so, as will be discussed in this article, would certainly be unfavorable in terms of health.

Souping vs. Juicing

Soups can satisfy

Soups may provide more satiety, or feeling of fullness, than juices. One study found that participants felt significantly less hungry after eating apple soup or an apple compared to apple juice. In another study, participants ate the same amounts of an apple, applesauce, or apple juice. Like the previous study, the apple and applesauce group felt significantly less hungry. They were then offered lunch 25 minutes later. They found that that the apple and applesauce group ate significantly less Calories at lunch than the juice groups. The apple group ate the least. Some soups in soup cleanses are served cold, sort of like applesauce.

The side-by-side

For easy comparison, one day of a soup cleanse, one day of a juice cleanse, and the dietary guidelines’ nutrient composition are lined up in the table below. I chose one day of a Reboot with Joe plan and one day of Soupure’s soup cleanse. The companies provided the nutrient information. The 2010 US dietary guidelines shown are based on a moderately active woman who is 31 to 50 years old.

Juice Soup DGs

*percentages do not sum to 100% as Calorie information was calculated from rounded gram values
**WHO 2002 recommendation

Juicing, compared to souping, has more sugar and carbohydrates, with less protein, fiber, and very little fat.  Both met guidelines for sodium intake and were low in calories. Souping is slightly above the US saturated fat goal.

Super sugary

The juice diet doesn’t meet recommendations for fiber and is very high in carbohydrates and sugar. More than half of the calories come from sugar! High-sugar diets are linked to unhealthy levels of insulin and triglycerides, but also more serious conditions, like non-alcoholic fatty liver disease and heart disease.

Juice diets are devoid of the nutrient-rich pulp and fiber-rich skin of fruits and vegetables. Pro-juicers typically claim that juicing “compacts” nutrients as it take several whole fruits or vegetables to make just one cup of juice. It is true that some nutrients may be present in higher levels, but so is sugar. Other vitamins and minerals that reside in the pulp would be lost. Furthermore, unlike whole fruit that has more fiber, the sugar in juice is in a liquid package.  Liquid sugar is absorbed more quickly and raises blood sugar to a higher level.  Below is a table comparing a cup of raw apple slices to a cup of apple juice.

Apple NF

Source: USDA Nutrient Database

As you can see, in the juice you’re getting more calories, more sugar, and less fiber. The juice does supply more potassium, but less vitamin C and folate.

Few fats

The juice diet provides very little fat.  An American Heart Association science advisory panel, led by Tufts University’s Dr. Alice Lichtenstein, examined diets less than 15% fat. They cautioned, in the short-term, these diets can lead to an unhealthy triglyceride level and decreased HDL or “good” cholesterol .

This juice diet is actually so low in fat that an essential fatty acid deficiency (EFAD) could be a concern. Your body can make some of the fats it needs for normal function, but others – essential fats – you must eat. EFAD is normally only seen in people receiving parenteral, or IV, nutrition who get too little fat. In parenteral nutrition, a minimum of 2-5% of Calories from fat are needed to prevent EFAD. It isn’t known, in food, what the minimum level is. Deficiency did occur in one man who ate a diet less than 7% fat for several months.

The Verdict

Variety is an essential part of a healthy diet. Many souping and juicing plans eliminate entire beneficial food groups like whole grains, lean meats, seafood, eggs, and dairy. This puts you at risk for nutritional inadequacies. It is clear that both souping and juicing don’t measure up as a long-term healthy diet.

If you are a healthy adult, there are (probably) no negative health effects of cleanse diets in the short term. If you are searching for a cleanse, it does appear that souping beats juicing. Souping offers a more ideal provision of sugar, carbohydrates, fats, fiber, and protein in terms of health.

Emily Finnan is a pediatric dietitian and a first year biochemical and molecular nutrition master’s student. While she does enjoy a good soup, she’ll stick to eating her fruits and veggies with a fork.

How Does a Ketogenic Diet Affect YOU? Part 3: C-Reactive Protein: A Marker of Inflammation

by Katie Mark

The latest craze surrounding the ketogenic diet has us further investigating whether or not a high-fat/low-carbohydrate lifestyle might be an appropriate dietary approach for some people. In this 3-part series (click here for part 1 and part 2), we’re evaluating how the ketogenic diet affects biomarkers.

The ketogenic diet is a very low-carbohydrate (<10% of total calories), moderate protein and high-fat (>70% of total calories) diet. After at least two weeks of keto-adaptation, the body’s energy source switches from glucose to fat.

In part one of “How Does a Ketogenic Diet Affect YOU?” we found studies suggesting that nutritional ketosis lowers fasting glucose and insulin levels and possibly increases insulin sensitivity. In part two, we investigated the impact of ketosis on cortisol. We found that a high-fat, carbohydrate-restricted diet may increase certain forms of cortisol, but blood cortisol levels are only half the story. Further research is needed to clarify the relationship between ketosis and an increase in certain forms of cortisol: the active form (cortisol), the inactive form (cortisone) and metabolites of cortisol from enzymatic breakdown.

Now let’s evaluate how the ketogenic diet affects C-reactive protein (CRP).

Increased CRP: Is there a need to worry?

C-Reactive Protein

C-Reactive Protein Model

CRP is considered a marker of inflammation. The liver makes CRP when inflammation in the body is present. High levels of CRP are influenced by genetics, high stress, exposure to environmental toxins and a sedentary lifestyle. Diet can also impact CRP levels, especially diets high in refined and processed foods.

There are two blood tests to measure CRP. The non-specific test indicates acute CRP levels that result from general inflammation in the body. The more sensitive measure is the highly sensitive CRP (hs-CRP) test, which accurately measures basal levels of CRP by measuring inflammation in blood vessels. The hs-CRP test is the accepted measure to determine the risk for cardiovascular disease (CVD).

Higher CRP levels signify a higher risk for developing CVD and abdominal obesity. Weight loss is known to decrease markers of inflammation such as CRP.

It is believed that a high saturated fat and very low carbohydrate diet (VLCARB) increases the risk for CVD. A study published in Nutrition Metabolism (London) compared a VLCARB diet to two low saturated fat, high carbohydrate diets to determine their effect on body composition and CVD risk. The isocaloric (similar calorie composition) diets were: very low fat (CHO:fat:protein; %SF 70:10:20), high unsaturated fat (50:30:20; 6%) and VLCARB (4:61:35, 20%). The study concluded that weight loss resulted in a reduction of CRP regardless of the dietary macronutrient composition. Yet, it is uncertain whether or not the macronutrient composition of a diet influences inflammation.

A study published in The Journal of American College of Nutrition found an increase in CRP in overweight women who followed a short-term low carbohydrate, high-fat weight loss diet. The study reported that an increase in CRP might have resulted from the oxidative stress caused by this type of diet.

Another study published in Obesity (Silver Spring) looked into the inflammatory response caused by a high-fat, low-carbohydrate weight loss diet (HF) by randomly assigning 19 overweight men and women to either an antioxidant (AS) or placebo (P) supplement. The objective was to see if the antioxidants vitamins C and E could decrease the inflammation reported in a HF diet.

CRP decreased 32% in the AS group and increased 50% for the P group; however, this was statistically insignificant. The HF diet did not decrease CRP within the short-term 7-day study even though other markers of inflammation decreased.

The study could not confirm if oxidative stress was causing the inflammation. It was concluded that further research is needed to determine the different CRP responses over the long term, especially while using antioxidant supplements. This is important considering most fruits and vegetables, which are low in fat, contain antioxidants.

The Verdict

A ketogenic diet may increase CRP levels, but weight loss reduces CRP levels. The reason for the increase in CRP is unclear. One plausible explanation is that low intakes of magnesium, vitamin C and other nutrients while on a ketogenic diet may lead to this effect. When magnesium is low, CRP increases. It has been reported that increased vitamin C intake may reduce high CRP levels.

An imbalance between anti-inflammatory fats (omega-3 fatty acids) and pro-inflammatory fats (omega-6 fatty acids) is another possible explanation. Polyunsaturated vegetable oils primarily contain the pro-inflammatory omega-6 fatty acids. Eating less grain-fed meats and chicken and more grass-fed meats and free-range chicken is also important to consider. Grain-fed animals have higher omega-6s whereas grass-fed animals have higher omega-3s. Omega-3s are anti-inflammatory and important for normal body functions, including regulating blood clotting and building cell membranes in the brain. Omega-3s are also suggested to protect against heart disease.

An elevated CRP level is never a good thing. If you are opting for a ketogenic diet, increasing magnesium and vitamin C intake as well as choosing grass-fed products may reduce CRP levels.

Katie Mark is a first year Nutrition Communication/Master of Public Health student who enjoys road cycling and traveling.

How Does a Ketogenic Diet Affect YOU? Part 2: A Deep Look Into Cortisol

by Katie Mark

Recent high hopes for high-fat diets have us further evaluating the ketogenic diet for a wider population. In this three-part series, we’re examining how the ketogenic diet affects biomarkers. Part 1 of this series investigated what ketosis does for fasting glucose and insulin. In Part 2, we look at how a ketogenic diet may affect cortisol levels.

High-fat…high cortisol…high stress?

Cortisol is considered the “stress hormone,” and it influences blood sugar levels, blood pressure, immune response, and stress response. Chronically elevated levels of circulating cortisol can hinder cognitive performance, disrupt sleep, impede immune function, increase abdominal fat, and cause blood sugar imbalances.

Studies have found that cortisol levels increase on a ketogenic diet, but some say the relationship between ketosis and high cortisol needs to be made clearer. First, chronically elevated cortisol correlates with metabolic syndrome, a group of symptoms such as high blood sugar, excess abdominal fat, and abnormal cholesterol levels that increase the risk for diabetes, heart disease, and cancer.

It seems possible that ketogenic diets may cause metabolic syndrome because higher cortisol levels suggest the onset of metabolic syndrome. However, this isn’t the whole picture: It’s also possible that there are multiple forms of cortisol, and their measurements mean different things.

Cortisol is measured in bodily fluids, including urine, saliva, and blood. Multiple forms of cortisol are measured from these samples: cortisone (the inactive form), free cortisol (the active form), and metabolites of cortisone and cortisol resulting from enzyme activity. Equally important, these levels of cortisol biomarkers can vary depending on the time of day.

A holistic understanding of cortisol metabolism relies on looking at the enzymes 11β-hydroxysteroid dehydrogenase (11β-HSD) and 11β-HSD1 (a subtype of 11β-HSD). 11β-HSD1 is found in every cell, but the highest amounts are found deep within fat cells. In fact, it does not matter if a person’s blood cortisol level is low, medium, or high because a highly active 11β-HSD1 will generate a high amount of cortisol inside cells.

Here is a breakdown of cortisol metabolism:

  • Production: 11β-HSD converts cortisol (active) to cortisone (inactive)
  • Regeneration: 11β-HSD1 converts cortisone to cortisol
  • Clearance: Other enzymes help metabolize cortisone and cortisol into metabolites

The cortisol profile of metabolic syndrome, which the ketogenic diet reverses, consists of:

  • High cortisol production
  • High cortisol clearance rates
  • High 11β-HSD1 expression in adipocytes and low 11β-HSD1 expression in the liver (the location that determines where and when cortisol is regenerated)

Now, let’s see how a 24-hour urine proxy is used for detecting cortisol. This proxy results in a less-than-clear picture because cortisol levels are affected by production, regeneration, and clearance. For instance, if clearance decreased or if regeneration increased, cortisol levels could go up if production stayed the same or lowered. This is analogous to simply measuring someone’s total cholesterol without observing LDL and HDL.

Take home message: levels may appear similar when there is a big difference in cortisol metabolism.

One study, published in The Journal of Clinical Endocrinology and Metabolism, used 17 obese men and randomly assigned them to an ad libitum (eat as much as you want) high fat-low carbohydrate (HF-LC) diet (66% fat, 4% carbohydrate) or moderate fat-moderate carbohydrate (MF-MC) diet (35% fat, 35% carbohydrate) for four weeks.

The study found a reversal of the previously described metabolic syndrome cortisol profile for only the HF-LC group: blood cortisol increased, clearance decreased and regeneration increased (due to an increase in 11β-HSD1 activity in the liver). According to the researchers, the ketogenic diet improved the cortisol profile because it was different from the cortisol profile seen in metabolic syndrome.

Furthermore, even though the MF-MC group lost a similar amount of weight, there was no change in 11β-HSD1 activity. This increase in 11β-HSD1 activity in the HF-LC group was independent of the differences in energy intake and weight loss because the same effect was seen in the controls.

A final component to note is that obesity is associated with high cortisol. However, the connection between obesity and elevated serum levels of cortisol has not always been a consistent connection.

Some people with high stress and lots of abdominal fat had normal or low levels of cortisol in their blood. Usually, chronically elevated levels of cortisol leads to increased adiposity; yet, there have been cases of people with high stress and high cortisol, but no obesity. And as we saw in “The Basics of the Ketogenic Diet,” the ketogenic diet has demonstrated effectiveness as a weight loss tool.

What’s the verdict?

We see that diet, especially a carbohydrate-restricted one such as the ketogenic diet, may increase certain forms of cortisol. But blood cortisol levels are only half the story—cortisol levels inside cells illustrate the other half. Also, cortisol will vary depending on the time of day, with levels highest in the morning. Caffeine, stress, and exercise can also increase cortisol levels.

Ultimately, further research is needed to better understand the connections as to why cortisol increases on a ketogenic diet and if cortisol levels are more affected by other variables, such as the activity of the 11β-HSD1 enzyme.

Katie Mark is a first year Nutrition Communication student from Miami, Florida. Due to Boston’s Snowpocalypse, she does not foresee herself living in Boston in the future, so she will return to South Beach following graduation.