Many studies have been published associating lack of sleep with increased body weight, but I have never read through the literature myself to explore the connection.

This week fellow scientist Matthew Constantin of Best Weight Loss Triumph gives us a thorough review of the science of sleep and weight gain.

Matthew Constantin, PhD, is a biologist and postdoctoral research scientist at Saint Louis University. Twice awarded research grants from the American Heart Association for his studies on cardiovascular disease, Matthew also has a keen interest in the related field of obesity treatment and enjoys explaining the latest scientific research on weight loss in a way that is easy for everyone to understand.

His website contains reviews of some of the so-called best rated weight loss programs and offers a savings coupon for Medifast, a clinically studied weight loss intervention.

Obesity and Reduced Sleep: Will Sleeping Less Make Me Fat?

By Matthew Constantin, PhD

We have long known that too little sleep causes fatigue and a slowing of neurocognitive functions, resulting in a variety of symptoms like slowed reaction time and difficulty concentrating. Recent research, however, has discovered a new result of reduced sleep: metabolic effects that include an increased risk of obesity [1].

Western society has seen a rapid rise in overweight and obesity in recent decades. Accompanying this widespread weight gain has been a significant and rapid decrease in the amount of time the average person spends sleeping.

While young adults were sleeping close to 9 hours each night at the beginning of the 20th century [2], this had decreased to less than 8 hours by the late 1960s [3]. The trend is continuing into the 21st century. As of 2005, 16% of American adults were getting less than 6 hours of sleep at night, up from 12% in 1998.

Sleep and Obesity: A Subjective Study

Science has linked self-reported sleep habits and obesity for a number of years, but the precise relationship between the two has been difficult to establish. Because obesity is a risk factor for a number of diseases that can negatively impact sleep, such as sleep apnea, asthma, depression, and arthritis, it is hard to know whether reduced sleep leads to obesity or obesity leads to reduced sleep.

To shed some light on this question, data collected from 1986 to 2002 in the Nurses’ Health Study (NHS) was analyzed [4]. Women in this study were asked to report their sleep habits and body weight every two years.

The results of the study suggest that women who self-report receiving less sleep are more likely to gain weight and are at an increased risk for obesity in middle-age. In 1986, when the first round of data was collected, it was found that women who reported sleeping 7 hours in a 24 hour period weighed 2.6 kg less than those who slept 5 or fewer hours, and 1.3 kg less than those who slept 6 hours.

This pattern continued over the following 16 years, with women who reported getting 5 or fewer hours of sleep weighing the most every time weight data was collected and those getting 7-8 hours of sleep weighing the least. In 2002, those in the 6-hour group had gained 7.2kg (15.8lb) and those in the 5-hour or less group gained 9kg (19.8lb), while those in the 7-hour group had gained only 4.8 (10.6lb) kg.

Other prospective studies have found similar results among both adults and children, but there are a couple of caveats. Because the information in the studies is self-reported, it is subject to inaccurate estimates by the reports. Many people overestimate sleep time when self-reporting. It is also unknown whether shorter sleepers are heavier because of an increase in fat or an increase in lean muscle—a distinction which makes a significant difference for health repercussions.

Sleep and Obesity: An Objective Study

In response to the limitations of subjective studies on sleep and obesity, two groups of adults aged 65+ (one of men and one of women) took part in an objective study that also looked at sleep duration and weight. Rather than relying on self-reported data, participants’ sleep patterns were assessed through the use of wrist actigraphy, which determines if a person is asleep or awake by measuring wrist movement.

This objective measurement of sleep duration confirmed the results of the subjective study, finding that reduced sleep was associated with an increased Body Mass Index (BMI) among both men and women. When compared with those getting 7-8 hours of sleep per night, average BMI of those who slept less than 5 hours was higher by 2.5 units in men and by 1.8 units in women. Moreover, men getting 5 or fewer hours of sleep were 3.7 times more likely to be obese, while women were 2.3 time more likely.

Increased weight doesn’t necessarily mean an increase in fat and its related health problems—more muscle also means more weight, but is generally associated with improved health. The objective study looked at this question and found that the increase in weight associated with reduced sleep was a result of increased fat rather than muscle. Overall percent body fat in those sleeping less than 5 hours was 1.7% greater than those getting 7-8 hours, and percent body fat in the trunk 1.9% greater.

Why Could Reduced Sleep Make You Fat?

Research has clearly shown that reduced sleep is associated with greater weight, but why does reduced sleep make a person fat?

One strong hypothesis is that less sleep leads to increased or altered food intake. Animals studies have found that sleep deprivation leads to elevated levels of hunger [5], with particular increases for high-fat and high-carbohydrate foods. This increased hunger with sleep deprivation may be a result of the corresponding change in hormones that regulate hunger, with gherlin levels found to increase and leptin levels to decrease.

Alternatively, rather than a change in feelings of hunger, increased food intake could be the result of increased eating even in the absence of hunger. Reduced impulse control and trouble delaying gratification are known consequences of sleep deprivation.

It’s also possible that simply being awake more often will lead to increased eating when food is readily available, especially if time awake is spent in sedentary activities that encourage snacking.

As S.R. Patel mentions in his 2009 review paper titled “Reduced sleep as an obesity risk factor”, there are several other possibilities that have been proposed. One is that the feelings of fatigue that are associated with sleep deprivation may result in a disinclination to exercise. Another is that reduced sleep results in a reduction in involuntary activities such as fidgeting, which are known to have effects on weight regulation [6].

Finally, acute sleep deprivation has been found to result in a drop in core body temperature, meaning your body needs to spend less energy in order to maintain thermoregulation with the surrounding air. This change in thermogenesis (the process of heat production) may encourage the storing of fat, although a recent study found no effect of sleep deprivation on resting metabolic rate.

Conclusions

Current evidence clearly shows that short sleep is associated with obesity, but a causal relationship remains unclear. Does a reduction in sleep lead to weight gain, or is there some other reason for the association? We don’t yet know for sure. But as modern society sets aside less and less time for sleep and becomes increasingly prone to obesity, it is a possibility that must be considered.

With so few effective ways to prevent and treat obesity, wouldn’t it be wonderful if simply sleeping a bit more could keep us both thinner and healthier?

References

1. Patel, S.R. Short sleep and obesity. International Association for the Study of Obesity. Obesity Reviews 10 (Suppl. 2), 61–68.

2. Terman L, Hocking A. The sleep of school children, its distribution according to age, and its relationship to physical and mental efficiency. J Educ Psychol 1913; 4: 269–282.

3. Tune GS. Sleep and wakefulness in normal human adults. Br Med J 1968; 2: 269–271.

4. Patel SR, Malhotra A, White DP, Gottlieb DJ, Hu FB. Association between reduced sleep and weight gain in women. Am J Epidemiol 2006; 164: 947–954.

5. Spiegel K, Tasali E, Penev P, Van Cauter E. Sleep curtailment in healthy young men is associated with decreased leptin levels, elevated ghrelin levels, and increased hunger and appetite. Ann Intern Med 2004; 141: 846–850.

6. Levine JA, Eberhardt NL, Jensen MD. Role of nonexercise activity thermogenesis in resistance to fat gain in humans. Science 1999; 283: 212–214.
Matthew Constantin

Tags: BMI, sleep

Photo by Robyn's Nest

Artificial sweeteners and sugar substitutes can be very appealing to people looking to cut their calories or control blood sugar, and I get a lot of questions about them. Generally I don’t recommend processed or sweetened foods and encourage people to break free from regular sugar consumption, but I recently discovered coconut palm sugar and decided to look into it.

Coconut palm sugar has garnered attention as being a low-carb sugar substitute that is both more nutritious and sustainable than typical granulated sugar. Because of its complex flavor it is also gaining a reputation in foodie communities, with establishments like the popular Samovar Tea Lounge in San Francisco switching 100% of its sweeteners over to coconut palm sugar.

Pure coconut palm sugar is a natural product made from the nectar of the coconut palm tree. There are several different varieties of palm (Palmyra, date, etc.), and “coconut palm” specifically refers to the coco nucifera plant.

Most of the “palm sugar” commonly sold in Asian markets is not pure coconut palm sugar but is blended with other fillers such as white cane sugar. Pure certified organic coconut palm sugar is sold under the brand name Sweet Tree in the US, and can be found at some natural food stores. It is also available online.

The information in this article applies only to 100% pure coconut palm sugar. Check your labels carefully.

Pure coconut palm sugar reportedly has a naturally low glycemic index (GI)–a measure of how food impacts blood sugar–which has led some people to claim that it is a valuable sugar substitute for people with diabetes or those looking to control blood sugar (the low-carb camp). Indeed, a lower GI may be a good indication that a food is safer for diabetics, though it is not a guarantee.

When I first saw that coconut palm sugar has a low GI I figured it would be composed largely of fructose, similar to the popular sweetener agave nectar (and high-fructose corn syrup). Fructose does not impact blood sugar because it is transported directly to the liver and converted to fat. For an explanation of this mechanism, check out Dr. Lustig’s video on the dangers of fructose.

I was surprised to find, however, that coconut palm sugar is reportedly very low in fructose, and its main sugar component is sucrose (aka table sugar). What confuses me is that the GI of coconut palm sugar is supposed to be 35, while the GI of sucrose is 64.

I feel obligated to qualify the numbers on coconut palm sugar, however, since I could only find a summary of how GI was measured and not the published study itself. Also, this information was only available on the website of a company that sells coconut palm sugar. This doesn’t mean the number is inaccurate, it just means I’d like to see the study repeated by another credible source or two before taking it as fact.

The number of calories in coconut palm sugar is almost identical to the number in regular table sugar and its closer relative, brown sugar. But coconut palm sugar is notably higher in various micronutrients, probably because it is less processed than industrial sugars.

But does anyone really eat sugar for health benefits?

There are a number of good reasons to consider using coconut palm sugar as a substitute for white or brown sugar in your kitchen. For me the most obvious benefit is that it tastes amazing, similar to brown sugar but with a rich complexity I’ve never tasted in industrial sugars.

Coconut palm sugar is also supposed to be substantially better for the environment, having been called the most sustainable sweetener by the Food and Agriculture Organization (FAO) of the United Nations (couldn’t find the original FAO report though).

Overall coconut palm sugar is a tastier and possibly healthier and more sustainable substitute for granulated or brown sugar. I wouldn’t go so far as to call it a health food, or even low-carb just yet. However it is a nice pantry addition for foodies concerned with sustainable products.

Substitute coconut palm sugar for traditional sugar at a 1:1 ratio in normal cooking and baking.

Have you tried coconut palm sugar? What do you think?

Tags: coconut palm sugar, diabetes, fructose, glycemic index, sucrose, sugar, sustainable, sweeteners

In a nation where obesity and health loom large in our public dialog, there is no escaping the simple fact that we eat too much.

On average Americans consume 500 more calories per day than we did in 1970 (more than we ever have), mostly in the form of refined and processed foods. This corresponds with a 25-30 pound increase in body weight and obesity rates near 30%.

Debates rage over the specifics of what is causing our weight and health problems, but it seems clear enough that the critical element is the amount of food we choose to put in our mouths.

But does everything we eat represent a true choice?

In his book The End of Overeating, former FDA commissioner Dr. David Kessler examines the role of the brain in eating behavior and the mechanisms involved in what he calls conditioned hypereating.

According to his findings specific combinations of sugar, fat and salt hijack the reward pathways of our brain and force us to behave more like food addicts than hungry organisms. This leads to a cycle of conditioned hypereating that makes the habit harder to break with each repeated episode.

But whether or not we are addicted to food is a point of debate. In my interview with Kessler, he made clear he does not use the word addiction for fear of oversimplifying conditioned hypereating. Our relationship with food is more complicated than it is with something like alcohol or tobacco because a human can live without cigarettes, but food is vital to survival.

When pressed to describe the neural differences between addiction and conditioned hypereating, however, Kessler conceded, “The fundamental circuits are the same.”

For this reason, treatment of conditioned hypereating can draw from the success of substance abuse treatments. These tactics involve cognitive and behavioral therapies we can use to train ourselves to override our instincts and adopt new behaviors in response to stimulus cues.

For conditioned and compulsive behavior, cognitive strategies are necessary because intuitive inclinations and “listening to your body” do more harm than good. If your body is telling you to have a cigarette, this does not mean it is in your best interest to do so.

At the FDA Kessler was instrumental in the fight to regulate tobacco, and now he believes some of the same lessons can be applied to the treatment of overeating.

“What took me a decade to understand is you need to change the valence of the stimulus.”

The positive emotional reaction associated with indulgent foods is at the center of our motivation to seek them out. Twenty years ago cigarettes had tremendous allure. But the FDA was successful at demonizing the tobacco industry, and the public no longer sees smoking as glamorous and attractive.

And smoking rates have plummeted.

Changing a conditioned behavior requires a fundamental shift in how we think about a stimulus. In conditioned hypereating the stimulus is food, which makes the task especially difficult, but not impossible.

To break the cycle of conditioned hypereating we must redirect our automatic response to the kinds of foods that cause us to overeat. Kessler calls these hyperpalatable foods, which are loaded with layers upon layers of sugar, fat and salt. The goal is to replace our automatic responses to these foods with different, equally enjoyable actions that are not detrimental to our health and do not reinforce compulsive behavior.

I asked Kessler what is the first step in controlling our eating habits and overcoming conditioned hypereating.

“I can tell you the last step. Change your relationship with food. If sugar, fat and salt are your friends, you will lose. You have to get to the point where that is not what you want.”

The End of Overeating outlines the four basic steps of habit reversal: awareness, competing actions, competing thoughts and support.

But Kessler believes the critical step is fundamentally changing the way we view what we eat, cooling down our emotional response to hyperpalatable foods. In essence, we must train ourselves to stop wanting what we believe we want.

According to the book, the first step in this transformation is becoming aware of the power food holds over us, which requires understanding how our brains work. We must recognize that when we are tempted to indulge, the urge is not generated internally but is a reaction to a cue that makes us respond automatically. You may think you are hungry, but really you are just reacting to an emotionally charged stimulus that tells you to eat.

Once you recognize a cue for what it is you have a brief moment to decide not to take the bait. To successfully divert yourself to another course of action you must have a plan ready in advance that allows you to do something completely different.

Considering alternative activities and the reasons you might prefer them can help you tremendously at this point of decision. Rather than focusing on the positive emotions you will experience by giving in to your desire for hyperpalatable foods, also remember the negative emotions that follow if you give in and the positive aspects of the alternative action.

For instance, it may help to remember that every time you get cued and give in, you are strengthening the neural circuitry that compels you to this behavior in the first place. If you even briefly entertain the possibility of indulging, you create a state of ambivalence that leads to torment, obsession and cravings. However, when you successfully divert your attention to another rewarding activity you have made a small step toward cooling down the positive valence of the food.

It is the state of mental torment and ambivalence that increases the positive emotional charge of a food, building and strengthening the neural reward circuitry that causes conditioned overeating. This may be one of the reasons dieting almost always results in long-term weight gain, since constant deprivation makes hyperpalatable foods more difficult to resist and creates severe anxiety.

Mentally, the best strategy to overcome conditioned hypereating is to develop new, positive associations with food that are independent of palatability–something you care more about than the fleeting reward of overeating. Kessler says this is a deeply personal process and must reflect an individual’s own set of values. For example, it helps some people to become vegetarian, while others value organics or local food. These decisions remove virtually all hyperpalatable food from the lives of people who choose these paths.

It also helps to develop aversions to hyperpalatable foods. Some may learn to demonize “Big Food,” while others turn away after educating themselves about health concerns. Developing a more sophisticated culinary palate can help make hyperpalatable foods less palatable. Kessler himself developed an aversion to over-sized portions, which he now sees as repulsive piles of sugar, fat and salt.

Developing positive associations with healthier foods while demonizing the hyperpalatable foods we have been conditioned to crave can fundamentally change your emotional response to stimulus cues. As you learn to recognize your brain’s response to cues, you can override conditioned behavior by consciously deciding to take alternative actions because you want to.

You will never win an internal battle with yourself. Instead use what you know about the brain’s reward system and give up trying to summon willpower to resolve the torment of conflicting desires. Reprogram your habits by closely examining your relationship with hyperpalatable food and begin making deliberate decisions that are consistent with your goals, breaking the cycle of conditioned overeating.

To read more about conditioned hypereating and habit reversal read The End of Overeating, by Dr. David Kessler.

OR

Download The End of Overeating audiobook from Audible

Have you read The End of Overeating? Have you overcome conditioned hypereating?

Tags: books, brain, David Kessler, The End of Overeating

1 lb Fat

Last week the New York Times and many other reputable news sources reported on a Canadian study that claims people with a normal body mass index (BMI) had a slightly increased risk of dying over a 12-year period than those with a BMI in the overweight range (25-29).

The use of the phrase “overweight was protective” landed this article just a hair’s width from being labeled Summer Tomato’s B.S. of the week on Friday. An observational study cannot determine cause and effect, as implied by the word “protective.” This study does not prove that extra body weight protects against all cause mortality, and saying so is irresponsible.

Studies (and reporting) like this have instigated wide-spread confusion about health and body weight. First people are told they are too heavy and should lose weight for health, then in the same breath they are told a little extra weight might not be so bad.

What is the average person supposed to believe? How should we act?

If you want to understand the facts it important to know exactly what the data does and does not say. Indeed, some studies (including one on Japanese men reported in the same issue of Obesity) have reported lower or equal risk of mortality for people with an overweight BMI compared to people of normal BMI (18.5-24). However, this is not the whole story.

First, the alleged benefit of being overweight has only been found in older individuals and does not apply to healthy, young people. Second, although it appears in some cases that overall mortality may be reduced, disease incidence is notably higher in overweight individuals compared to people of normal weight.

To point, a study in the most recent issue of Obesity (same journal, 2 weeks later) examines the relationship of BMI with many measures of cardiovascular disease in healthy, athletic men. In this study, those on the lowest end of BMI in the normal range (18.5-22.5) had a much lower risk of dying from or developing cardiovascular disease than normal weight men with a slightly higher BMI (22.5-25).

Men with the lowest healthy BMIs also had lower risk of hypertension, lower cholesterol and half the risk of diabetes. While the length of this study was only 7.7 years (compared to the 12 years reported in the Times story), there were more than double the number of participants (28,776 vs. 11,834).

(Why did this story not make the news? My guess is that it makes for a less compelling storyline and people would rather not hear it.)

Mortality is certainly an important measure in any study, but it is arguably not the most relevant endpoint. Disease and excess body weight can severely impact quality of life, particularly for older individuals (as illustrated by another study in the latest issue of Obesity). While I cannot speak for everyone, it seems probable that quality of life is equally if not more important than longevity alone. Thus it is questionable how much stock to put into studies that ignore these other factors.

It is also critical to remember that BMI is a measure that was designed to describe people at a population level, not as individuals. While large cohort studies can tell us useful things about relative risk, they are not directly applicable to individual people.

The inconsistency of the data related to BMI and mortality may in fact be an indication of its inadequacy as a general measurement. Remember that BMI represents a ratio between height and weight, making it possible to compare people of various body sizes. Normalizing for height may, however, be deceptive.

Decades of data on caloric restriction consistently show that smaller body size (irrespective of body fat levels and, possibly, BMI) is associated with longer life and decreased risk of nearly all diseases. This is true in all animals from yeast, to worms and flies, to mice and monkeys. While humans are certainly different from all these model organisms, there is tremendous evolutionary precedent indicating smaller body size as the best for health.

The principle of parsimony tells us the simplest hypothesis–that smaller body size is beneficial–is probably correct. Substantial evidence must be accumulated before this hypothesis can be rejected, and I have yet to see that data.

Furthermore, while the research on the risk of overweight may be slightly ambiguous, the data on obesity is not. It is painfully clear that the dangers of obesity are profound and on par with those of smoking cigarettes. Overweight is a necessary step to becoming obese, and according to the National Population Health Survey nearly a quarter of Canadians who were overweight in 1994/1995 were obese by 2002/2003. Since overweight is still a substantial risk factor for becoming obese, misleading public health messages about the benefits of body fat are especially dangerous.

As a consumer of information, the most important thing you can do is be skeptical of what you read. Just because something is printed in the New York Times does not make it true. In fact, many of our most trusted sources of health information do not base their recommendations on rigorous scientific thinking, which is probably the reason for the health disaster we are currently facing.

Thanks to Jan from Quest for Health for sparking this discussion.

What does your gut tell you about the relationship between health and body fat?

Tags: BMI, body fat, body mass index, caloric restriction, mortality

Collards, Carrots and Lentils

A new study published yesterday in the Archives of Internal Medicine suggests that both weight loss and risk factors for heart disease can be improved following a vegan version of the low-carb, high-protein Atkins diet.

The “Eco-Atkins” diet focuses primarily on soy, nuts and wheat proteins (gluten) to increase the amount of vegetarian protein in the diet. Carbohydrates were restricted to 130 g/day, which is on the higher end of most low-carb diets. All starchy foods such as bread, baked goods, potatoes and rice were eliminated. Carbohydrates were provided in the form of whole, intact grains (barley and oats) and low-starch vegetables.

In a small (47 participants), short-term randomized controlled trial, this diet lowered bad LDL cholesterol by 20%, without negatively impacting good HDL cholesterol (statin drugs improve cholesterol levels by 30%). The diet also substantially lowered blood pressure and other markers of cardiovascular disease, such as triglycerides and apolipoprotein B.

The original meat-based Atkins diet has been shown to be effective for temporary weight loss (after 1 year the effects of the Atkins diet are diminished), but cardiovascular risk factors such as LDL cholesterol and blood pressure are not substantially improved under the traditional Atkins regimen.

Interestingly, a traditional Atkins-style diet based on animal protein was not used as a control in this study, so a true comparison of the diets cannot be made using the present data. Instead the researchers chose a control diet representative of a typical high-carb, low-fat vegetarian diet that included eggs and dairy products. Both diets tested in this study represented a 60% decrease in total calories.

Because of the study design, we cannot conclude that this diet is more effective than the Atkins diet for health, though you would predict it would be if future studies made this comparison. On the other hand, it does seem that a plant-based high-protein diet is more effective at improving health than a high-carbohydrate lacto-ovo vegetarian diet, at least in the short-term in a highly controlled environment.

This study took place over the course of 4 weeks, and all the food was provided for the particpants by the researchers. Thus, compliance in the program was very high. It is not clear if the participants would have had the same level of success if they were instructed to provide their own food to comply with the dietary programs.

Despite this, satiety levels were notably improved in the high-protein group and it would be expected that the increase in satiety would encourage greater compliance in a free living situation.

A small four week study, however, tells us very little about the effectiveness of this diet. While it is possible to improve risk factors such as cholesterol and blood pressure in such a short period of time, disease outcome is the true measure of a successful diet. Also, this study did not test the feasibility of the Eco-Atkins diet in the long-term, and it is likely many dieters would object to a strictly vegan regimen.

Interesting points raised by this preliminary study include:

• Plant-based, high-protein diets may be more effective at improving cholesterol and other cardiovascular measures than traditional lacto-ovo vegetarian diets.
• Short-term weight loss is primarily determined by the number of calories consumed, not macronutrient content.
• Low-carb diets that include intact whole grains and plant-based protein can be effective at improving both weight and cardiovascular risk factors in the short-term.
• Plant-based high-protein diets can increase satiety compared to high-carb vegetarian diets.

However, many questions must be addressed before this diet can be recommended to individuals trying to improve cardiovascular measures and lose weight.

New questions:

• Can the Eco-Atkins diet be maintained in the long-term by normal individuals?
• Does the Eco-Atkins diet continue to improve cardiovascular risk factors including weight loss after 4 weeks?
• What would result from this study if beans and lentils were used instead of soy and gluten?
• Does the Eco-Atkins diet improve disease outcome?
• Does the Eco-Atkins diet extend life?
• Does the Eco-Atkins diet affect quality of life?
• Can these effects be attained through other diets that include some animal protein, more whole grains or more fat?
• Is the effectiveness of the Eco-Atkins diet affected by an individual’s level of insulin resistance?
• Can adding fish further improve the results of the Eco-Atkins diet?
• Can a further reduction in carbohydrates improve the results?
• Will you get these same results if the study is NOT funded by the soy industry?

In summary, the results of this study are interesting and encouraging, especially for those of us who think both carbohydrates and meat should be limited in a healthy diet. I very much look forward to future studies exploring this idea.

What concerns me most is the lack of marine omega-3 fatty acids (fish) in the Eco-Atkins diet, which could potentially improve cardiovascular measures even further. Fish is also important for cognitive health and may lower cancer risk.

I am also worried that a strictly vegan diet would not be feasible in the long-term for many Americans. Moreover, it is not necessarily the healthiest option available. Vitamin B12 deficiency is a particular concern, but could be addressed with supplements. Generally, however, I do not recommend relying on supplements for optimal nutrition.

Finally, this study was funded by a company that makes soy and gluten products. Personally I would have prefered to see these protein sources used in combination with other things such as beans and lentils. Many people question how much soy can be safely consumed and gluten intolerance is more common than ever, so wouldn’t it be interesting to know if there were safer alternatives? It really annoys me to see science being influenced by industry funding.

What do you think of the Eco-Atkins diet?

Tags: beans, eco-Atkins, gluten, high-protein, lentils, low-carb, soy, vegan, vegetarian