Is Long-Term Weight Loss Possible?

I’m working on a conference presentation for health care providers on helping adolescents lose weight. I called my husband the other day a little frustrated that I didn’t have the solution to the world-wide obesity epidemic to share with the audience. Obviously, I have some delusions of grandeur. 

Throughout the week, combing through the research really depressed me. There are so many articles that talk about the obstacles to long-term weight loss and so few that provide promising solutions. No one really has the answer to this question. A lot of diet books claim to know, but the authors are just trying to make a buck. Decoding the mystery to long-term weight loss is a little like figuring out why Arnold Schwarzenegger would cheat on Maria Shriver with the housekeeper--totally baffling. 

An article that was just published by Marc-Andre Cornier (2011) adds a layer of frustration to the problem. Dr. Cornier writes about how, as people lose weight, their bodies fight to regain it. The person’s metabolic rate slows. (This makes sense as smaller people burn less calories than bigger people.) After weight loss people also feel hungrier, aren’t satisfied after a meal, and tend to fidget less. The human body doesn’t like weight loss and fights tooth and nail to get back to its previous chubby state.

Long-term weight loss is so rare that scientists are able to keep track of people who have managed this in the National Weight Control Registry (NWCR). In fact, less than 10% of people who lose weight are able to keep it off for 5 years (Cornier, 2011). The 5,000 or so people in the NWCR all have some things in common; they maintain a low-fat, low-calorie diet; eat breakfast every day; weigh themselves at least once a week; watch less than 10 hours of TV per week; and exercise about an hour a day (NWCR, 2011). All of this is well and good, but it doesn't show what motivates them to do all of these things, when 90% of weight losers aren't able to stay motivated.

Just when I was ready to throw in the towel, I had a little glimmer of hope. Researchers at the Urban Policy Institute discovered some stark differences in obese teens who lost weight over the course of time and obese teens who gained weight during the same time. They found that all of the teens who lost weight had an a-ha moment. There was a tipping point that changed their path. 

One teen had a track coach who complimented her running, but told her that she would be even faster if she ate better. Another teen had been worried about his grandmother's diabetes around the same time his doctor brought up his weight and risk of diabetes. Another teen had an a-ha moment at the neighborhood basketball court saying, “I sat there, and I watched other people play…. They sweat a lot, but they don’t get tired, and I get tired… I was like, I don’t wanna be like that for the rest of my life.” (Lieberman, 2009) After these a-ha moments, these teens made significant lifestyle changes. In contrast, there were few life-altering moments in the group of teens that continued to gain weight. 

I had a turning point like this when I quit smoking 10 years ago. I was at a drag queen Abba concert even though I had a head cold. I had been trying to quit smoking for a while and had been resisting buying packs of cigarettes. I really wanted a cigarette that night and I bummed one off some guy. The cigarette tasted awful, as any of you who have smoked a cigarette with a cold could have predicted. I had the epiphany that smoking was a disgusting habit that night and that was my last drag of a cigarette.
  
Unfortunately, none of these a-ha moments occurred during unique situations. Every smoker brakes down and has a cigarette when sick and the cigarette, no matter how much the smoker is craving it, tastes repulsive. Why don't all smokers quit when this happens? Many overweight people have a health scare or a moment where they feel bad about their weight. What was different about the teens in the article?


What do you think? Stay tuned for part two.


Cornier, M-A. (2011). Is your brain to blame for weight regain? Physiology and Behavior. E-pub ahead of print.

Lieberman, A., et al. (2009) Why some adolescents lose weight and others do not: A qualitative study. 101(5); 439-447.

High-Fructose Corn Syrup vs. Sugar (Part 2)

When something goes awry in society, be it an increase in autism or obesity, or 90s fashion trends reentering teens' closets, it is human nature to want to blame a culprit.


Researchers at George Mason University are studying parents’ decisions to immunize their children and looking at what one of the researchers calls the “Jenny McCarthy Effect.” Ms. McCarthy, of 1990s-Playboy-model-turned-TV-hostess fame, leads the campaign that claims childhood vaccines cause autism. Many people have chosen to skip immunizing their kids, even though studies show that immunizations do not lead to autism and protect children from diseases.


The researchers were surprised by who was most susceptible to the “Jenny McCarthy Effect.” People who were highly educated, intelligent, and well-off were more likely to choose to forgo immunizing their children because of concerns about autism. In fact, the more educated a person, the more likely they were to fall victim to the “Jenny McCarthy Effect.” Poorer, less educated people routinely listened to their doctor’s advice (and the literature) and immunized their kids.


I feel like high-fructose corn syrup (HFCS) has become a little like the childhood-immunization-leading-to-autism hype. Educated, intelligent people are swearing off all foods with HFCS based on pretty shaky scientific knowledge.


I really want to tell you that HFCS is the root cause of our obesity epidemic, because that would be the socially acceptable thing to do. It would also be such a simple solution to the battle of the bulge and, boy, could we use a simple solution. Unfortunately, the research out there is pretty far from this conclusion.


Nearly everything I’ve come across in reputable journals like the American Journal of Clinical Nutrition, Nutrition and Metabolism, and The Journal of Nutrition, say that sugar and HFCS work the same way metabolically. An article in The Journal of Nutrition even goes far enough to say “Misconceptions about high-fructose corn syrup abound in the scientific literature, the advice of health professionals to their patients, media reporting, product advertising, and the irrational behavior of consumers.” (White, 2009) Studies have not found that HFCS is unique in the way it leads to obesity, predicts obesity, or that eliminating HFCS from the food supply would decrease obesity (White, 2008).


It’s true that as HFCS has increased in food, the obesity epidemic has also increased. There’s more food available and people are eating more of everything, especially fat and starches (White, 2009). The two things are correlated, but it doesn’t appear that one caused the other.


There is one study out of Princeton that showed that rats that were fed HFCS overwhelmingly became obese, while those who ate sugar did not (Parker, 2010). This is interesting, but I would like to see more studies on humans in this area. If the science goes this way, I will be sure to update my blog post.


Don’t get me wrong, I’m in no way calling HFCS a health food or advocating purchasing products that contain it. It’s processed and calorie dense and has all of the makings of an unhealthy food-like substance. I just no longer think it’s a magic obesity potion. In doing this research, my view of the unhealthiness of HFCS didn’t really change, but my view of sugar did. Table sugar does all of the same bad things to blood sugar, triglycerides, and our svelte figures as HFCS, so if you’re going to rid your cabinets of HFCS, might as well throw out that sugar too.


I feel that all of those “No HFCS!” and “Now with real sugar” labels are the epitome of misleading advertising, as are most health claims on packaging. So, here’s my advice:


• Try to avoid savory foods with any kind of added sugar, be it HFCS, brown sugar, evaporated cane juice, agave nectar, or plain-old sugar. It’s just adding extra calories.
• Use HFCS on a food label as a warning sign that the product is ultra-processed, high in calories, and contains other unhealthy ingredients.
• Don’t go crazy banning HFCS. If you really like something every once in a while that contains it, have it. You will still be able to zipper your jeans tomorrow.




Sources:


Parker, H. (March 22, 2010). A sweet problem: Princeton researchers find that high-fructose corn syrup prompts considerably more weight gain. Retrieved online from http://www.princeton.edu/main/news/archive/S26/91/22K07/.


White, J.S. (2008). Straight talk about high-fructose corn syrup: What it is and what it ain’t. American Journal of Clinical Nutrition. 88(suppl):1716S-1721S.


White, J.S. (2009). Misconceptions about high-fructose corn syrup: Is it uniquely responsible for obesity, reactive dicarbonyl compounds, and advanced glycation endproducts? The Journal of Nutrition. 1219S-1227S.

Throw Down: High-Fructose Corn Syrup vs. Sugar

My husband and I were eating walnut-chocolate chip pancakes with Aunt Jemima Butter Light Syrup a few weeks ago. (I know, it’s the nutritional equivalent of supersizing a Double Whopper Meal and then ordering a Diet Coke.) During breakfast, I read the back of the syrup label and  high-fructose corn syrup (HFCS) was staring at me. If not for my husband’s pardon, Aunt Jemima would have found herself headed to a landfill that day. (Just kidding; I would have recycled her.)

HFCS has been on many of our nutritional no-no lists for a few years. I saw a blog post a few weeks ago that mentioned HFCS. In the comments, someone wrote “What’s the matter with HFCS?” She might have well of asked “What’s the matter with genocide?” The readers went crazy, citing “research” studies that gave HFCS magical obesity-causing properties.

Background

HFCS gradually began replacing sugar in beverages and processed foods during the 1970s and 80s. It was cheaper and, since corn is grown domestically, not susceptible to the pesky little episodes of civil unrest prevalent in the tropical environments where sugar cane is grown. Because it is already in liquid form and corn is highly subsidized by the government, HFCS makes producing vats of soda much, much cheaper.

Nutritional Makeup

The nutritional make up of HFCS and sugar is pretty similar. HFCS is comprised of 55% fructose, 42% glucose, and 3% “readily hydrolysable polymers of glucose” (your guess is as good as mine). Table sugar (sucrose) has a 50/50 fructose to glucose ratio. Both substances are heavily refined and striped of nearly all nutritional value. Honey has a similar ratio to the other two sweeteners (White, 2008).

 

The HFCS Hater’s Argument

HFCS haters feel that HFCS reacts differently in the body than sugar and disproportionately causes obesity, especially the dreaded abdominal obesity. They also point out that as HFCS use has increased, so have the waistbands of Americans.

 

The Defense

Much of the defense of HFCS comes from ads and “expert” testimony produced by the Corn Refiners Association that claim that HFCS is identical to sugar. It has all of the markings of a big business moneymaking conspiracy. Watch the commercial below.

Why It’s Not So Cut and Dry

I’ve been a member of the I Hate HFCS Club for a bit, but a few things recently have made me want to take a closer look at this. The first red flag came when I saw a friend drinking a Pepsi Throwback. In the midst of the HFCS controversy, Pepsi came out with a soda made with real sugar accompanied by some borderline health promoting advertising. Wait, so soda is healthy if it’s sugar and not HFCS? I don’t think so.

I’m not particularly proud of the second reason I started doubting the evilness of HFCS. I was searching for a video on youtube and came across this one produced by the Corn Refiners Association. Normally, I would write this off as a super-biased video from an association that has everything to gain from hooking Americans up to intravenous HFCS. My issue here was one of ego. One of the experts in this video was the medical director at the George Washington University. I happened to go to grad school at GW. If you know anything about GW, you know that I will be paying for my education there until my hair is completely gray and robots rule the earth. I can’t let myself think that a representative from my alma mater would flat out lie about HFCS and still send them so much money every month. Besides, we’re “the” George Washington University. That means we’re super smart.

So, the battle of HFCS vs. sugar is open. Do you think HFCS is worse than sugar? Vote here. Stay tuned for the science on both sides.

Sources:

White, J.S. (2008). Straight talk about high-fructose corn syrup:  What it is and what it ain’t. American Journal of Clinical Nutrition. 88(suppl):1716S-1721S. 

Fitting Into Those Skinny Genes (Part 3)

We are absolutely not made to
handle the toppings bar at
FroZenYo.

FroZenYo, a self-serve frozen yogurt Mecca of yumminess, opened in my neighborhood last month. You walk in, pick up an oversized cup, fill it with fro yo, add toppings, and then weigh the monstrosity to pay per the ounce. After you pay, “free” hot fudge beckons from beyond the register. With all of those options, it’s pretty hard to limit yogurt flavors and toppings. The sheer quantity of hard-to-resist treats leads me to make some pretty interesting flavor combinations. Coconut and pistachio yogurt with berries, wet nuts, Oreo pieces, and hot fudge, anyone? Oh well, guess I’ll blame my inability to resist all of these sweet, crunchy, gooey delights on my genes.

Since FTO and similar genes make food more attractive and lower a person’s ability to resist yummy, sweet, and fatty foods, these genes definitely make living in our society harder. It wasn’t always so. Hundreds of years ago, this genetic predisposition to eat large quantities of fattening foods would have helped us survive. Throughout history, humans ate when the harvest came in or when someone from the village killed a large animal. There were periods of feast and famine. The drive to chow down kept us alive through the harsh winter. Now we power through the cold weather with venti hot chocolates, big bowls of meaty chili con queso, and non-stop streaming Netflix.

Technology has created the perfect obesity storm by making food-like substances easier and cheaper to produce. Food (or something that closely resembles it) is always around us. (Ever walked past Chipotle at 3:00 in the afternoon? There’s a long line. What meal is that exactly? Linner? Or maybe dunch? Who knows, but I need that 1,100-calorie burrito the size of my head!) Technology also enables us to stay perfectly still for long periods of time, save for pressing buttons on the remote control, smart phone, computer, etc.

These changes in our society have happened really fast, and, as a society, we’ve gained weight really fast…

… and evolution happens slowly. So, on the nature vs. nurture debate, I’m going to have to side with nurture.

Genes don’t directly affect our weight; they affect how we interact with our environment. Simply, our bodies aren’t made to live in our current society and we are going to keep getting fatter unless our environment and culture change. I’m fully aware that I’m not going to solve the obesity epidemic with this blog post, but this is how I think we can set ourselves up for success in this sedentary, food-crazed culture:

Step 1: Boycott buffets and all-you-can-eat situations. FTO and similar genes don’t allow most of us to handle them. Hey, 18% of noncarriers lost control when confronted with a Chinese buffet too. Buffets are bad news. Willpower is a myth and, unless famine is imminent, stay far away.

Step 2: More importantly, cut back on eating out all together. If we’re going to change the obesity epidemic in one generation as Mrs. Obama has promised, there needs to be a return to healthy home cooking.

Step 3: Vote for policies/politicians that work to make healthier foods cheaper and more available than junk food. To make it work, healthier foods, like farmer’s market produce, would have to be subsidized and unhealthy foods, like soda, would have to be taxed. Current government policies are setting us up for fatness.* I’m personally working to create a generation of conspiracy theorists at the college where I teach health. The truth is out there. Trust no one.

Step 4: Don’t keep crappy food in your house. Just skip the chip aisle. You know you can’t avoid it if it’s in the house. Blame it on FTO.

Step 5: Exercise for at least an hour a day. FTO carriers who exercise weigh less than those who don’t exercise (Mitchell, 2010). Duh.

Step 6: Breastfeed. Some new research shows that being breastfed for at least a month may lessen the effect of FTO in childhood (Dedoussis, 2011).

How else could we change our food environment and culture? Comment!

Sources

Dedoussis, G.V., et al. (2011). Does a short breastfeeding period protect from FTO-induced adiposity in children. International Journal of Pediatric Obesity. 6(2-2):e326-335.

Mitchell, J.A., et al. (2010). FTO genotype and the weight loss benefits of moderate intensity exercise. Obesity (Silver Spring). 18(3):641-643.

*To be described in a future post.

Fitting Into Those Skinny Genes (Part 2)

As those of you who voted guessed, our genes most definitely play a part in our weight, but not for the reason most people think. Our genes don’t affect how many calories we burn. Like in the mini experiment in Part 1, the amount of calories our bodies burn at rest is dictated by sex, weight, height, and age. Our genes work in a much more interesting and kind of scary way; they change the way we look at food.

If you’ve ever scanned the websites about the secrets of “naturally” skinny people, you’ve probably noticed that a lot of the secrets have to do with the way these skinny minis behave around food. They eat small portions; they don’t treat hunger as an emergency; they fill up on fruits and vegetables. Yes, naturally skinny people all have those things in common. They also look pretty similar genetically, especially on a gene called Fat Mass and Obesity-Related Gene (FTO). (Nope, I’m not even kidding about the name of this gene.)

 

Researchers at the Bute School of Medicine in the United Kingdom screened for FTO on a group of over 2,700 4- to 10- year-old children. If a child inherits FTO from both parents, the child is described as homozygous, meaning she has two copies of the same gene. Scientists use the shorthand AA for people with two copies of the FTO gene. People who only inherent one copy of the gene are heterozygous; and are labeled with the shorthand AT. Those without the gene are labeled TT. In this study, the scientists also measured the children’s height and weight, waist and hip circumference, and body fat.

Of the children in the study, 14% inherited two copies of FTO from their parents (AA). Nearly half (49%) inherited one copy of the gene (AT). The remaining 37% did not inherent any copies of the gene (TT). Those with one (AT) or two copies (AA) of the gene were more likely to be overweight and had an average of four pounds more body fat than their counterparts. Those who carried two copies of the gene (AA) were heavier than those with just one copy (AT).

Here’s the kicker. The carriers of the gene (AA or AT) burned an average of 84 more calories per day than those who didn’t carry the gene (TT). Both those who carried the FTO gene (AA or AT) and non-carriers (TT) burned about the same amount of calories as the researchers predicted based on their basal metabolic rate; that is, the bigger kids burned more calories than the smaller kids and boys burned more calories than girls.

It all came back to food. During the second part of the study, the researchers measured the children’s food intake. The children were fed a buffet lunch with ham, cheese, carrots, cucumber, potato chips, rolls, crackers, raisins, chocolate candy, grapes, orange juice, and water. Interestingly, all of the children ate about the same amount of food; however, the gene carriers (AA and AT) consumed 16% more calories and 30% more fat than the noncarriers (TT). The carriers of the gene chose the more fattening and higher-calorie foods, like the candy and chips, while the noncarriers gravitated towards the foods with lower calories like the fruit and vegetables (Cecil, 2008).

I absolutely love Nutella and its chocolaty, hazelnutty deliciousness. At a previous job, I kept a jar of it at my desk. I was towards the bottom of the jar and alone in my shared office. I don’t know what came over me, but a few minutes later, I had my hand jammed into the jar so I could get every last morsel of goodness into my mouth. That is until a coworker walked in and said, “What the hell are you doing?” It wasn’t until then that I realized that Nutella was on my chin, shirt, and forearm up to my elbow. Researchers call this phenomenon loss of control eating. It happens to all of us, but it happens more often to FTO carriers. On a research trip to the Chinese buffet, 37% of carriers, both AA and AT, lost control with all the moo su pork in sight. Only 18% of noncarriers (TT) got to the point where they lost control (Tanofsky-Kraff, 2009).

Since FTO was first discovered in the early 2000s, data from over 80,000 people have been analyzed. The probability that FTO’s affect is due to chance is 1.2 in 1,000,000,000,000,000,000,000,000,000,000 (Frayling, 2007). Repeatedly, studies have found the same thing—those with one or two copies of the FTO gene weigh more and eat more than those who do not carry the gene and this trend has nothing to do with metabolism (Speakman, 2008). Of course, FTO isn’t the only gene that has an effect on obesity—it’s just shown the biggest effect to date (Li, 2010).

So, why are we seeing this obesity epidemic now? Has our DNA changed? Stay tuned for Part 3 for more riveting genetic information.

Cecil, J.E., Tavendale ,R., Watt, P., Hetherington, M.M., Palmer, C.N. (2008). An obesity-associated FTO gene variant and increased energy intake in children. New England Journal of Medicine. 359(24), 2558-2566.

Tanofsky-Kraff, M., Han, J.C., Anandalingam, K., Shomaker, L.B., Columbo, K.M., Wolkoff, L.E., Kozlosky, M., Elliott, C., Ranzenhofer, L.M., Roza, C.A., Yanovski, S.Z., Yanovski, J.A. (2009). The FTO gene rs9939609 obesity-risk allele and loss of control over eating. American Journal of Clinical Nutrition. 90(6), 1483-8.

Frayling TM, Timpson NJ, Weedon MN, et al. (2007). A common variant in the FTO gene is associated with body mass index and predisposes to childhood and adult obesity. Science. 316, 889-94.

Speakman, J.R., Rance, K.A., Johnstone, A.M. Obesity (Silver Spring). (2008). Polymorphisms of the FTO gene are associated with variation in energy intake, but not energy expenditure. 16(8), 1961-5.

Li, S., Zhao, J.H., Luan, J., Luben, R.N., Rodwell, S.A., Khaw, K.T., Ong, K.K., Wareham, N.J., & Loos, R.J. (2010).  Cumulative effects and predictive value of common obesity-susceptibility variants identified by genome-wide association studies. American Journal of Clinical Nutrition. 91(1):184-90. 

Fitting Into Those Skinny Genes (Part 1)

Do our genes play a role in weight?

Some coworkers and I got into a heated discussion about whether some people draw the genetic short straw when it comes to weight or if people from heavier families are more likely to pack on the pounds because they are raised on Quarter Pounders and Häagen Dazs. We went back and forth talking about friends who ended up skinny in overweight families, friends who ended up overweight in skinny families, and, more often, people who look a whole lot like the rest of their families.

All of these stories came with the added bonus of eating up a good chunk of my morning at work (shhh, don’t tell my boss and Curtis, if you’re reading this, I’m totally making this up); however, this really didn’t get us any closer to solving the nature vs. nurture debate. Sorry, we couldn’t have been of more help, field of psychology.



So, I did what the geek-girl inside of me needed to do and set up a mini experiment. There are a couple of ways to measure metabolic rate (a.k.a. how many calories we burn a day). The more accurate way is to measure a person’s basal metabolic rate (BMR). BMR is measured in a dark room after 8 hours of sleep and 12 hours of fasting. Needless to say, we didn’t choose this option as it would have been a little awkward and cramped for us all to sleep in the conference room. My hair also works its way into a fauxhawk overnight and I really didn’t want my coworkers to see me like that. 

Instead, we had a company come in with equipment to measure our resting metabolic rates (RMR). RMR is way less cumbersome and only requires 4 hours of fasting (and no coffee!). The tech had each of us lie down in a reclining chair (one at a time, of course); she put a clothespin on our noses, and then has us breathe into a contraption for 15 minutes.

Afterwards, we all shared our results. With a few exceptions, the number of calories each of us burned a day at rest was as expected based on our sexes, weights, heights, and ages. Caloriesperhour.com provides a calculator that gave us our comparison RMRs. As a general rule, the taller, heavier, and younger a person, the more calories she burns at rest each day. Men burn more calories than women. #sonotfair

Based on RMR readings, it seems like our bodies try to compensate for extra weight by burning more calories. If a bigger person burns more calories, why are they bigger? And why do some people seem to be immune to weight gain?

The question of the week is: Do you think genetics play a role in weight? Click here to vote, or put your vote in the comments section below if you have rebelled against the facebook machine. Voting is open through Sunday, July 3^rd.

Case Closed on Whole Milk vs. Skim Milk

It's a hung jury.

Every Saturday morning from April through November, I visit my neighborhood farmer’s market primarily to pick up my week’s supply of Strawberry Yo-Light from Blue Ridge Dairy. The ingredients in this delightful creation are pasteurized low-fat milk, organic strawberries, nonfat dry milk, organic sugar, fruit pectin, citric acid, and live and active cultures. Sometimes the guy at the farmer’s market sells out before I get there and I have to go with the Honey Yo-Light. (Then I shake my fist towards the heavens and I ask myself, “Why does he only bring five containers of the good stuff? Why?!?!?!” If you’re reading this Mr. Blue Ridge Dairy, let’s get going on the strawberry this week, ‘kay?) Either with the strawberry yogurt or the somewhat inferior honey, I feel like my weekday breakfast of oatmeal, light yogurt, fruit, and a vat of coffee is super healthy. Well, maybe not so much the vat of coffee.

This week, I picked up some fresh mozzarella to make a caprese salad to accompany our pre-triathlon carb-loading pasta. The mozzarella was made with whole milk and it was delicious. I can’t imagine that a fat-free mozzarella would have complemented the farmer’s market fresh, local basil and tomatoes quite so well. So, it was light on the yogurt and the real thing on the cheese, and I felt pretty darn good about it, based on both my taste buds and the science.

That’s right, the case of whole vs. skim ended with a hung jury. Readers were split 50/50 on the case and scientists leaned towards low-fat dairy by a thin margin. Many studies gave skim milk an advantage in promoting a healthy weight with the caveat that people who take care of themselves gravitate towards lighter choices in all areas, including dairy. Some studies also found that skim or whole didn’t matter, especially in moderate amounts. There were too many other possible explanations for the results in the pro-whole milk studies.

So, in sorting through the e-confusion, we’re going with a mixed-method approach:

• Light yogurt wins. It’s just as creamy and good and is way lower in calories. Let’s face it—most of us don’t need extra calories. (Check the back of Fage Whole Milk Greek yogurt if you want a good shock to the system.)
• Non-fat cheese doesn’t melt (other than “cheese food”—yuck!) and is pretty unappetizing and ultra-processed. I would go with a 2% or part skim for extra-cheesy dishes like enchiladas, or a full-fat cheese as a treat, but in small quantities.
• I’m having the hardest time with straight-up milk, mostly because I don’t like the way milk tastes and I can’t imagine sitting down with a glass of it. I also don’t like the concept of drinking calories (unless said beverage begins with a “w” and ends with an “ine”). My recommendation here is to drink what tastes better in moderation if you love milk. If you don’t love the taste of milk, eat yogurt, or get your calcium from food sources like broccoli (my favorite food), leafy greens, or canned salmon (Sound gross? Try these salmon cakes with fiery salsa. You’ll be a believer!)

Just like anything in life, moderation is truly the way to go. After all, we don’t eat fat or calories; we eat food. And, Mr. Blue Ridge Dairy, please remember my strawberry yo-lite this weekend. Thank you very much.

Note: Some of you noticed that I didn’t touch organic vs. conventional milk, raw milk, or dairy alternatives (soy, almond, etc.) in this post. That’s a blog for another day.