Genes, Obesity, and the Snowball Effect.

In The Secret Life of Fat, Sylvia Tara documented the effects of genetics on one’s propensity to gain weight and difficulty to lose it, all else being equal. (In fact, her personal experiences with these effects are what motivated Dr. Tara to investigate the genetics-fat link in the first place.)

Recent research, led by David Meyre at McMaster University, has found nine genes that combine into what the researchers call the snowball effect.

“These genes,” Meyre told Science Daily, “may, in part, explain why some individuals experience uncontrolled and constant weight gain across their life, despite the availability of different therapeutic approaches.”

This is fascinating and important research that highlights the genetic pre-disposition to obesity and points at future models to detect genes and work towards individualized lifestyle programs to prevent obesity.

We caught up with Dr. Meyre to find out more.

ScienceToLiveBy: What specifically motivated this study into the genetics of obesity?

Dr David Meyre: While the average body mass index has reached a plateau in Western countries such as the United States, extreme forms of obesity are still on the rise. The origins of super obesity are still poorly understood (is it genes, environment, both?).

This is the reason why we studied the effects of 37 well-established obesity genes on body-mass index in 75,230 adults with European ancestry using innovative statistical methods (conditional quantile regression and meta-regression models).

We found that nine of the 37 genes (24%) make individuals gain more weight if they already have a high body mass index. The effect of these genes is amplified by four times, if we compare the 10% of the population at the low end of the body mass index, compared to the 10% at the high end. The plausible explanation is that there are interactions between these snowball obesity genes and risk environmental factors.

STLB: Explain the “snowball” effect? Is that a snowballing of the number of these nine genes that an individual has? Or having all nine means the higher your BMI gets, the faster it will continue to increase?

DR MEYRE: The number of bad copies (0, 1 or 2, one inherited from your father, one inherited from your mother) for each of these 9 genes is determined at conception. It can be comprised between 0 and 18 obesity risk copies depending on the individual.

Your second proposition is right. The bad copies at these genes make you gain weight, and when you get heavier, they make you gain even more weight (a vicious circle or snowball effect). The effect of these genes on weight gain can be four-times stronger if you compare the 10% lighter and 10% heavier people.

STLB: Are there certain individual or subsets of the nine genes identified that combine for part of the effect — or is it all nine that have to work together?

DR MEYRE: The nine genes do not interact with each other, so their effect is independent and sums up. The more obesity risk copies of the genes you inherit from your parents (from 0 to 18), the more you gain weight.

STLB: Is there an available way individuals can screen for these genes, these SNPs?

DR MEYRE: The effects of these nine genes is modest (it may contribute to 2% of body mass index variation in population) so genetic testing is not relevant for now. However, genetic testing of these snowball obesity genes may become relevant when we identify all of them (there are probably several hundred snowball genes disseminated on the whole genome). This may take couple of years.

STLB: What treatments, if any, do you see that could be developed based on knowing these all these genes and the snowball effect?

DR MEYRE: Prevention may be a more adequate option here. We already know that certain of these snowball obesity genes interact with lifestyle factors such as your diet, physical activity, sleeping habits, soda and alcohol drinking consumption habits.

The strategy in the long run may be to identify the subset of people who cumulate many of these snowball obesity early in life, and to propose a personalized lifestyle intervention program based on the genetic profile that minimizes the effect of these genes and maintains individuals in the low body mass index range.

STLB: What studies do you have planned to follow up on or compliment this study?

DR MEYRE: The next step is to generalize our discoveries in populations with non-European ancestry. More than 270 obesity genes have been recently identified in European, East Asian, South Asian, African, Native North American, South American and Pacific Islander populations, and more snowball obesity genes are likely to be found in the future.

We are also developing novel statistical and informatics methods to screen the entire human genome to track-down novel snowball obesity genes. Another important goal is to identify the specific lifestyles that interact with the snowball genes. The next steps are to improve the prediction, prevention and care of snowball obesity at the population level.

The paper and abstract are available here. Read more about Dr. Meyre’s research here.

Microbiome and disease: infant risk for asthma may be more than genetic.

As readers are aware, here at ScienceToLiveBy.com we take the gut microbiome very seriously. And we’re particularly interested in how the microbiome is linked to disease. We are continuously learning how diet and behavior can influence the microbiome and health outcomes.

Late last year, a University of Alberta study showed that the family risk for asthma, usually passed from mothers to babies, may be caused by more than genetics. The study, led by Anita Kozyrskyj, found a significant reduction of the Lactobacillus family of microbes in Caucasian baby boys born to pregnant women who had asthma. According to the findings, there is strong evidence that maternal asthma during pregnancy may be associated with an infant’s gut microbes.

Dr. Kozyrskyj told Science Daily, “Our discovery, with more research, could eventually lead to a preventative approach involving modifying the gut microbiome in infants to reduce the risk.”

The lab is also looking into whether certain sex-specific risks towards being overweight are related to changes in infant gut microbiomes. We caught up with Dr. Kozyrskyj of University of Alberta to find out more about their research.

ScienceToLiveBy: What specifically motivated the research into the gut microbiome – asthma link? Had you pursued other links prior to this study?

Dr. Anita Kozyrskyj: I was motivated to study the gut microbiome-asthma link by the well-established fact that maternal asthma affects infant birth weight in a sex-specific manner. Some of this evidence was published by Dr. Clifton at the University of Adelaide.

STLB: Any hypotheses as to how gender differences may be causing the sex-specific effects on gut microbiome?

DR. KOZYRSKYJ: Male fetuses and those of mothers with asthma are more likely to have problems swallowing amniotic fluid, which is essential for intestinal absorption of nutrients. Lactobacilli have been detected in amniotic fluid.

STLB: Other coverage of your research cautioned against pro-biotic treatments, did you mean in the infants after birth, or for women with asthma before or during pregnancy?

DR. KOZYRSKYJ: I believe the article stated that it was too early for parents to act on my findings. Certainly lactobacillus-containing probiotics have been tested during pregnancy and in the infant after birth for their effectiveness in reducing onset of allergic disease. Probiotic efficacy is strongest in preventing allergic eczema and weakest in preventing asthma from developing. However, it’s possible that lactobacillus supplementation efficacy is sex-specific.

STLB: Are you looking at other gut-gender-disease links in pregnancy?

DR. KOZYRSKYJ: Male infants who are treated with antibiotics are more likely than girls to become overweight. We are also looking into whether this sex-specific risk for overweight is related to changes to infant gut bacteria.

STLB: What studies might you be planning for follow up?

DR. KOZYRSKYJ: The plan is to link these findings to the development of allergic disease in the CHILD birth cohort as children get older. CHILD cohort children are currently being assessed at age 5 for the presence of asthma and allergies.

Journal Reference:

  1. Petya T. Koleva, Hein M. Tun, Theodore Konya, David S. Guttman, Allan B. Becker, Piush J. Mandhane, Stuart E. Turvey, Padmaja Subbarao, Malcolm R. Sears, James A. Scott, Anita L. Kozyrskyj. Sex-specific impact of asthma during pregnancy on infant gut microbiota. European Respiratory Journal, 2017; 50 (5): 1700280 DOI: 10.1183/13993003.00280-2017

 

Probiotic berries

Probiotics: The year in review

It’s that time of year to start looking back and wrapping up the news — good or bad — in our favorite research areas.

What happened in the world of Probiotics in 2017?

Perhaps our favorite development comes from the National University of Singapore (NUS). As reported in Science Daily, the NUS has developed a specialty beer that incorporates the probiotic strain Lactobacillus paracasei L26. This friendly organism helps regulate the immune system and has the ability to neutralise toxins and viruses.

We can imagine the marketing — “Tastes Great!” “Less Toxins.” Okay, you have to be a certain age to remember the iconic “Tastes Great – Less Filling” Miller Lite ads. (In all fairness to us, they did bring back the tagline as recently as 2008 )

Creating the beer wasn’t as easy as you might think. Acids in beer kill off bacteria, so the brew process needed tweaking and trial and error with different strains of bacteria robust enough to survive. As of August, the student entreprenuers did not have a commercial agreement, but we’ve heard that a Japanese beverage company was interested.

Next up: allergies.

As any sufferer knows well, seasonal allergies disturb your sleep, lower productivity at work, home, and school, cause stress and embarrassment. In summary, they make life miserable.

And current allergy medications have fun side effectslike dry mouth and drowsiness. Yay!

Probiotic BerriesIn March we learned of research at the University of Florida that showed promise in relieving the symptoms of hay fever. A double-blind, placebo-controlled, parallel, randomized clinical trial, showed that a combination probiotic improved “rhinoconjunctivitis-specific quality of life during allergy season for healthy individuals with self-reported seasonal allergies.”

Translation: allergy sufferers felt better!  Something to try out next spring.

Guts, brains, and IBS depression.

A study released in May added to the data on the microbiota-gut-brain axis, providing evidence that bacteria affect behavior.

Say the researchers, “This study shows that consumption of a specific probiotic can improve both gut symptoms and psychological issues in IBS.”

How does it work to reduce depression? Researches used fMRI to asses brain activation patterns, and measured fecal microbiota, urine metabolome profiles, serum markers of inflammation, neurotransmitters, and neurotrophin levels. The probiotic reduced responses to negative emotional stimuli in multiple brain areas, including amygdala and fronto-limbic regions. The improvements were associated with changes in brain activation patterns that indicate that this probiotic reduces limbic reactivity.

That is, the priobiotic not only improve the gut, but directly improve negative brain symptoms.

High blood pressure.

An MIT study showed how a strain of intestinal bacteria can stop a high-salt diet from inducing inflammatory response linked to hypertension.

Before we get into it, this is not a license to eat fast foods and take a probiotic antidote!

Rather, if you have been enjoying a too high-salt diet then in addition to changing it, you could add the right probiotics to further protect yourself from the effects.

Yogurt and berriesSo what’s going on? Well, a high-salt diet shrinks the population of a certain type of beneficial bacteria. As a result, pro-inflammatory immune cells grow in number. These immune cells have been linked with high blood pressure, although the exact mechanism of how they contribute to hypertension is not yet known. In the study, the probiotic Lactobacillus murinus lowered the immune cell populations and hypertension was reduced.

Again, the obvious conclusion here is to avoid a sustained high salt diet. But this study and others like it reinforce the important links between diet, gut microbiome, and disease.

Age and microbiota.

At least two studies looked at changes in gut microbiota and how this relates to aging.

In one study, the researches transplanted the microbiota from the guts of old mice into young mice, causing inflammatory responses in the young mice. Inflammatory response are linked to age-related conditions such as stroke, dementia and cardiovascular disease.

Why aging tends to lead to negative imbalence in “good” and “bad” bacteria is not fully known. But the study suggests such imbalance may be on the cause side rather than the effect side of some of the inflammatory conditions that lead to age-related diseases.

Another study of “ridiculously healthy” elderly subjects confirmed that they have the same gut microbiome as healthy 30-year olds. Researchers could not identify whether this is cause or effect — do healthy elderly have good microbiomes or do good microbiomes keep people healthy into old age — but it does show that microbiome could at least be a marker for predicting health into old age or even lead to treatments for age-related conditions.

Too much of a good thing?

Before you pile on the probiotics to your already healthy diet, make sure you’re not overdoing it.

A study at the University of New South Wales exploring the link between gut health and brain function had one surprising result. For the subjects (aka rats) put on a poor diet, the diet caused memory and other brain issues. And, the good news, the probiotics helped stop the losses. That’s the good news.

But — there’s always a but — rats in the “healthy-diet” group not only saw little additional benefit to added priobitocs, the supplements may have led to some memory impairment.

What this shows is how it is important not to overdo any good thing. And that it is critical, though difficult, to determine which beneficial microbes are absent before treating with probiotic supplements on top of a healthy diet. As always, much of the research our microbiomes is directed at teasing out cause and correlation: when can we prevent and heal and when can we merely predict and otherwise act. Do changes in the biome predict disease or prevent disease?

As always, you should test and measure — if you supplement and feel worse, reduce or stop. This requires good record keeping and journaling to track what foods and supplements are working. And, as always, check with your health care provider before making any changes to diet or supplementation.

When do we eat?

I first learned of Intermittent Fasting (IF) from The Secret Life of Fat. In it, Sylvia Tara described how she used IF in her arsenal of tactics to reduce body fat and increase lean muscle mass. This sent me of on a Quest for Fasting.

I found that in addition to longer overnight fasts like Dr. Tara used, practitioners defined a variety of IF routines.

Quest for FastingThere is the long intra-day or overnight fast like Tara’s. These can use early dinner, late breakfast, or both to increase the fasting time.

There are also 5:2 fasts, where you eat for five days and then fast (or calorie restrict) for two days. And a monthly variant, where you calorie restrict for 5 days a month.

Every other day fasts alternate eating and fasting days. One routine employs a 24-hour fast (from the end of dinner on Monday until the start of dinner on Tuesday). Another option is to alternate eating days with 36-hour fasts (from end of dinner on Monday until breakfast Wednesday). Clearly, there is an infinite variety of protocols.

What a difference a day makes

One fasting fact really struck me: the liver stores enough glycogen to supply the body with its glucose needs for at least 24 hours after feeding.

That forced me to think about why we eat when we do.

Empty PlateIt’s natural to think about our food needs on a daily basis. The day is an obvious cycle for us Homo sapiens. Because of this, we think about our Daily energy needs — such as the Daily Minimum Requirements. This leads us to plan and eat in daily “chunks.” Each day we want to meet our calorie and nutrient goals. Then the timer resets overnight and we start over the next day.

But is this daily planning optimal? Worse, is it detrimental?

Let’s imagine, for kicks, a shorter timeframe. What if the way we thought about eating, from our vocabulary to the planning, research studies, and recommendations were hourly instead of daily? We wouldn’t talk about needing 3,200 calories a day, but rather about getting our 200 calories per waking hour. And we’d eat that way. Planning each hourly meal. That’s right, lunch every hour!

Sure, that’s kind of absurd.

But is our daily framework causing a version of this same “eating too frequently” problem? Turns out research supports this conclusion. We simply don’t need to eat every day. I’ve already mentioned that we store enough to supply our glucose needs for twenty-four hours without eating again. But what else justifies spreading out the eating?

What’s the downside of constant eating?

Insulin response is a big factor here. Near constant eating, with a short break to sleep, never lets insulin levels and the important follow-on processes fully reset. Think of those NiCad rechargeable batteries. When you don’t fully drain them all the way before recharging, what happens? Their performance degrades.

EvolutionThere’s an evolution-versus-modern-life dynamic at play here. Between seasons, droughts, fires, monsoons, migrations, and other forces of nature, foods weren’t always available in abundance all year in our pre-history. Three square meals a day (plus some snack bars) was a luxury that just didn’t come that often. Thus, natural selection has left us with systems that are attuned to packing away food (as fat) for our use in the down times.

Think about it. If not eating for a day made us lethargic, light-headed, and dysfunctional, how would we ever have survived as a species? The first drought or winter season would have killed us all.

When we feed all the time, we disrupt the body’s store-and-release process. Our constant eating barely taps our system of stored energy (fat). Like that rechargeable battery, we’re draining a little and topping off every day. And never letting the full system get exercised.

That’s in the best of cases. In the worst case, constantly high insulin levels lead to insulin resistance which cascades into a host of well-known issues like obesity and diabetes.

The modern response to putting on weight, though, has been to limit our daily caloric intake — trying to manipulate the calorie input and output: deficit to lose weight, balanced to maintain weight.

Obesity trends suggest that this doesn’t work. In fact, constant eating at reduced calories triggers different responses than does not eating all. This is the well-known metabolic slow-down and other effects. Fasting is potentially a more evolutionary approach to managing calories and energy supplies with the way our bodies are designed to work, without the side effects of daily calorie restriction.

Better insulin management is just one benefit fasting for longer periods. Studies show improved functions from memory to concentration, to physical agility.

But fasting is sooooo uncomfortable!

With the idea of working towards an every other day routine, I started with a single 24-hour fast. Like most people, I didn’t know what I was in for.  Fear of hunger and discomfort can make fasting hard to start.

Tips to start a fast protocolMy initial 24-hour fast was tough. No denying it. I couldn’t stop thinking about fasting, which of course kept me focused on food — or the lack thereof. I got headaches and a little weak-kneed. But I made it.

Several days later, I fasted again. This time it was much easier. And easier again two days later. Now I’m on an every other day 24-hour fast.

(A side benefit of the 24-hour routine: you don’t skip a dinner, so it’s easy to work into family or social life.)

Hangry, anyone?

Hunger is a big fear for anyone trying to fast. With hunger, though, you quickly realize something: it’s more in your habits than in your gut.

I noticed that much of the hunger cycle is about habit. For what seems like forever, I’ve had a coffee and a snack when I got to the office. Like Pavlov’s dog, getting to my desk was like a bell ringing. My brain told me it was snack time. Once you break these habits and change the stimuli, it is much easier. (See the tips above.)

What about exercise? Not a problem. I’ve been able to do my usual high-intensity-interval-training (HIIT) routine during fast days without a hitch. You have to feel it to believe it: you will not be lethargic or hungry on fast days. And despite the common wisdom, you will not start “burning muscle” when you fast. The body protects the brain first and the muscles second — remember, you need both to find that next meal in the wild. If you do resistance training, you can build muscle on a fasting routine.

So, when do we eat?

The research, and my experience, is starting to show that the answer is: far too often.

Disclaimer: I’m not your doctor. I’m not anyone’s doctor. This material is for information purposes only. Speak with your medical professional before starting any diet or exercise program.

Yo-yo dieting

Is yo-yo dieting killing you?

We all know the story. And the stats. Some 90% or more of weight loss diets fail, and many dieters actually end up heavier. What’s going on?

Are these dieters just lazy? People who’ve never had a weight problem would say so. “Eat less. Move more.” It’s so simple, right?

Short answer: no.

There are a number of factors that help us unpack aphorisms like “eat less, move more” and “calorie in, calorie out.” In short, it’s all relative to your unique factors: food processing genetics, microbiome, age, hormones, gender, viruses, and more.

At some level, yes, within each individual’s body situation, “eat less, move more” may be true.  But how much less and how much more?

The details are too many to discuss here (it would take a book!). So take our word on it for now.

How does this relate to yo-yo dieting?

One key finding is that when you lose fat—like that first 10 pounds that you quickly dropped on your latest diet attempt—your body signaling changes. This is because key signaling hormones are produced by fat itself. The fat goes down, the signaling slows, and profound changes occur.

These changes make you feel hungrier and burn less calories than people never heavier than your new weight. Feeling hungrier, in this case, doesn’t just mean a little bit of tummy growling.

Your brain is going to react differently to food. Seeing food, smelling food, even thinking of food, will all cause stronger emotional reactions than they would have at your starting weight. You will crave more calorie-dense foods. Furthermore, depending on the foods you now eat, you may alter your microbiome. And you’ll feel too strained to exercise as much as you’d like to (because you’re feeling the need to overcome that slower metabolism).

As all these forces align, you fall off the program. The weight goes back up, like that yo-yo.

So you try again on another plan. Same thing. Only the effect is greater. Each time you lose and gain you risk further disturbing your bodies signaling around hunger, digestion, fat storage, insulin sensitivity and a host of factors. On top of it all, your will power, confidence, and mood are taking a beating too.

Would you be better off never trying?

Not knowing what you were getting in to, frankly, yes. The mission was doomed to fail. And the more you yo-yo, the worse your health is getting. It’s literally killing you.

Losing weight and getting rid of fat really strikes a nerve in us modern humans. And we seek silver bullets. Unfortunately, many dieters put more research into choosing a flat-screen TV or a new laptop than they put into choosing a diet plan. (TV manufacturer’s—maybe you should claim to change people’s lives in 10 days.)

To break the yo-yo cycle, you have to put the work in up front and along the way.

First, barring outright snake oil, some people will respond to a particular diet and exercise plan. Keep in mind, though, that your friend who got great results was lucky to have hit on a diet that was aligned to their factors. That doesn’t make the same plan right for your context.

So think about what worked for you and what didn’t in the past. Look for patterns.  Can you eat a moderate amount of carbohydrates—grains and veggies—as long as you don’t overdo the sugar cookies? Or does being in the same room as a banana make you gain weight?

Next, exercise. You’ve heard that building muscle mass will raise metabolism and help you burn fat. True. And you’ve read that high-intensity interval training (HIIT) is a super fat-burner. True again. But, you recall, that when you have done intense exercise, weights or HIIT, it made you so hungry that you overcompensated on the calories. It could be that low-intensity steady state (LISS) workouts will be better for you in the long run.

The point is, you have to research, learn, and experiment to understand what factors are most important for you.

Only then can you get off the yo-yo train.

Virus Factor

The Virus Factor: Is there a connection with obesity?

Virus Factor

Wired.com recently detailed the AD-36 virus and it’s correlation with obesity in humans. This discovery is a fascinating tale of its own, as one medical doctor turned fat researcher pursued answers to help his patients.

Dr. Nikhil Dhurandhar followed his father’s footsteps and ran a clinic Mumbai, India to treat overweight and obese patients. Dhurandhar was constantly frustrated that he could not produce answers that would keep his patients from re-gaining weight. “Patients kept coming back,” he recalls.

A serendipitous tea with a family friend and veterinary pathologist gave Dhurandhar a clue that upended his life on a new journey, one might say an obsession.  The pathologist friend was investigating an epidemic in the poultry industry, and something he said sparked a connection in Dhurandhar. The virus causing the illnesses had an interesting symptom–the infected chickens had fat deposited in the abdomen. Could there be a link?

Through several years, a move halfway across the globe, and a healthy dose of skepticism from the research community, Dhurandhar pursued his research, ultimately identifying that a human adenovirus, AD-36, was correlated to higher fat and obesity in humans.

How does a virus lead to fat?

According to Dhurandhar’s research partner, Richard Atkinson, there are three ways that it could:

  • Increased uptake of glucose from the blood
  • Increased creation of fat molecules through fatty acid synthase
  • Creation of more fat cells to hold all the fat by committing stem cells into fat

“So the fat cells that exist are getting bigger, and the body is creating more of them,” says Atkinson.

Read the Wired.com article.

Get the full story in The Secret Life of Fat, now available online and in bookstores.

 

 

 

 

Fat Baby

This little girl couldn’t stop eating, what happened next changed our understanding of fat

Layla appeard to be a healthy newborn. But as she grew into her first year, something changed. Layla would finish a bowl of food and cry until she was given another. Her parents knew this was unusual, but suspected it was a temporary stage of development.

As Layla continued to grow, however, so did her appetite, and before long she was obese. The family tried to reduce her weight gain by cutting calories and encouraging more activity. It was to no avail, because Layla became inventive at finding food. She would burrow through the trash and break into locked cabinets. Once she even forced open a locked freezer and ate frozen fish. Even when they succeeded, limiting Layla’s food intake didn’t help her lose weight, it only served to increase her violent outbursts and her desperate search for food.

Fat BabyDoctors tested her for everything they could think of: a thyroid disorder, pituitary and adrenal glands abnormalities, Cushing’s syndrome, Prader-Willi syndrome, Bardet-Biedl and Alstrom’s syndromes. But all tests were negative. No one was sure what was causing Layla’s ferocious drive to eat and nothing seemed able to stop her.

Layla, it seemed, was destined for a lifetime of obesity.

At about that time, a very interesting study was being conducted that shed light on Layla’s problem. Researchers found that a group of mice with a specific gene mutation had unstoppable eating behavior and grew obese. The mutation was in a gene that made a hormone produced by body fat, and when the mice were given this hormone, they lost weight and not muscle or bone, just fat.

Researches found that this hormone sent the signal to the brain to stop eating. Mice with the gene mutation became obese because they always felt hungry–they never got the signal. Today, we call this hormone leptin and know that it plays a role in humans, as well.

One expert on Layla’s case (Dr. O’Rahilly) learned of this discovery, and he noticed many similarities to the child’s case. Like the mutated mice, she was extraordinarily obese, had an unstoppable urge to eat. He tested Layla’s leptin levels, and found he was correct — Layla was a human version of the mutation, she had no leptin! At last, there was an explanation for why Layla could not stop eating.

What happened next was no less than amazing. When O’Rahilly started administering leptin to Layla, her appetite decreased significantly. As O’Rahilly recalls, “She was eating a quarter compared to what she was normally eating. She went from being a completely focused eating machine into a normal kid.”

Further research would show that leptin not only reduces appetite but is also involved in metabolism. In addition to eating like gluttons, mice without leptin tend to move less and burn less fat. Without leptin, Layla was unable to burn fat normally, which is why even when her calories were restricted she could not lose weight.

Hormones matter much more to our weight and metabolism than we often give them credit. Before starting a diet it’s important to understand how our hormones really work. Here’s one example why: High fructose foods reduce the effect of leptin, and can lead to leptin resistance. With leptin resistance we are more hungry and gain weight.

There are many things you can do to promote fat-burning hormones such as growth hormone and testosterone and decrease the effects of fat-hoarding ones such as insulin. I discuss all of this at length in my book, The Secret Life of Fat.

Elements of a Paleo diet

One reason why Paleo doesn’t work for everyone (and how to burn stubborn fat)

Based on the fact that humans have only recently undergone massive changes to our diets, the paleo diet cuts the refined sugars, grains, and legumes most of us now eat in abundance, but which our bodies aren’t suited for. It’s a diet that works wonders for many people, but there are a certain few for whom paleo doesn’t live up to its expectations. So if paleo is fundamental to our human core, why would it work for some but not for others?

Elements of a Paleo diet

Elements of a Paleo diet

One issue lies right in the theoretical basis of the paleo diet — our DNA. Humans grow and adapt to our environment. We experience variations in our genetic code that alter us over time, and they are not the same for everyone. So whatever genetics our ancestors had a few thousand years ago, they are not necessarily what we all still carry today. Some variations make it easier or harder to see results with the Paleo diet, or any diet plan.

Once we account for some of these variations, however, Paleo can work again.

One issue lies right in the theoretical
basis of the paleo diet — our DNA.

Take for example recently identified genetic variation known as FTO. An FTO variant has been shown to increase desire for energy rich fattening foods. An appetite for high calories foods is bad enough, but this FTO variant also leads to another outcome — it creates more fat cells! A study at MIT showed that those with the FTO variant gene also create more white fat cells (those which hoard fat) than brown fat cells (those which burn energy to produce body heat). So the net effect of the FTO alteration is a larger appetite and a higher propensity to create white fat cells. It’s a combination that would make it hard for anyone to lose weight!

Our genes are changing on an ongoing basis. And for the last few centuries that we’ve had farming and industrialized food our genes and bodies have changed further. Paleo is a sound and sensible approach for most. But if you find paleo isn’t quite working for you, the answer may be in your genes.

Fortunately, researches who study obesity genes say that exercise doesn’t just combat fat but also the effects of “fat” genes. For instance, research at Mt. Sinai in New York showed that 30 minutes of activity 5 days per week reduced the effect of the FTO variant by 27%. Dr. Ruth Loos, the lead researcher of the study, mentions that the exercise “doesn’t have to be overly vigorous, as long as you start to sweat,” which means even biking, gardening, or going for a brisk walk will work. Of course, that still leaves 73% of the gene’s effect intact. To ratchet up the fight, research at Pennington Biomedical Research Center in Louisiana showed that more intense activity will blast through genetic predisposition to fat. It seems that once we enter a specific range of exercise, the body kicks in to lose fat no matter what our genes want.

But that’s just exercise, fasting is another way to burn stubborn fat. Fasting will induce growth hormone (which peaks at night) and amplify your fat burning pathways. Extend the overnight fasting period from 5 pm to 11 AM the next day to increase growth hormone production and fat burning.

You should also look to remove obesogens from your diet — these foods mimic estrogens and can lead more fat. They are found in plastics, pesticides, and preservatives and even some plants such as flax and soy. You could be following the paleo diet to a T, but if you’re exposed to obesogens your chances of maintaining fat are much higher.

The Secret Life of Fat

Stubborn fat is a reality for many. You may have biological reasons why you don’t lose weight as quickly as your neighbor. However, you can make almost any diet successful, as long as you understand your fat first — including all the ways we get fat and how fat fights to stay on us. I explain all the unknown facts about fat in The Secret Life of Fat.

Bones

What would happen if we had no body fat?

We willingly spend billions of dollars to win the war on body fat every year, and yet it always seems to come back, and more resilient than ever. Why is that? Why is that fat just keeps fighting back? Because as much as you think you want to lose fat, your body still isn’t convinced it should.

Benefits of FatThere are good reasons for your body to accumulate and store fat. Fat is a cushion of energy in times when we go too long without eating. It’s the safety net that keeps your heart, brain, and muscles going when we need more fuel than what’s immediately available.

But more than just a reserve of calories, fat plays a critical role in many body functions because it releases hormones. This discovery, in the 1990s, led fat to be reclassified as an endocrine organ. It turns out fat does some great things for us, though we don’t normally recognize them. What does fat do for us?

Enables Puberty — Ballerinas, who are often super skinny due to their strict lifestyle, will miss their periods or even delay puberty until after ending their career. This puzzled doctors and scientists until they found that fat makes both estrogen and leptin which are needed for puberty and reproduction.

Strengthens Our Bones — Fat isn’t just important for puberty, it’s also important for our bones. It turns out that body weight is a better predictor of bone mineral density, a measure of fracture risk, than age.

Boosts Our Brain Size — The health of our fat (yes, your fat can be sick or healthy!) affects our brain size. Patients with defective fat (fat that’s doesn’t make sufficient hormones) have smaller brains. Individuals with anorexia, who are characterized by having minimal fat, also see a decrease in brain size and volume. On the other hand, people with too much visceral fat are at risk of dementia. The health of our fat is directly connected to the health of our brain!

Enhances Our Immune System — On top of cushioning our most sensitive organs and keeping us warm, fat (through leptin) also strengthens our immune system and assists in wound healing. In fact, anorexics have weaker immune systems and heal more slowly than those with normal fat levels.

Helps us live longer — In times of sickness a little extra fat may prove beneficial. For instance, while fat has been blamed for heart attacks, strokes, diabetes, and a host of other serious illnesses, researchers are finding that low fat levels may make us even more vulnerable to death from those conditions. In many studies, being overweight actually lowers mortality from disease!

Without body fat, life as we know it wouldn’t exist. Perhaps fat is not quite the enemy we always make it out to be. At the very least, it is certainly more complex than the typical one-size-fits-all diet makes it out to be.

Yes sumo wrestlers are obese — but are they unhealthy?

By any standard, the sumo wrestler would be considered obese. Sumo wrestlers weigh in the range of three hundred to four hundred pounds and ingest 5000 to 7000 calories a day, including a lot of fried food. While their diet is low in processed foods and sugar no one could argue that their diet is healthy.

And yet they don’t suffer from afflictions normally associated with obesity. Their plasma glucose and triglyceride levels are normal. Even their cholesterol levels are low. How is it that they can escape the health effects of excess weight in ways the rest of us can’t?

The question puzzled doctors for years, until a study using computer tomography imaging looked at the fat deposits on sumo wrestlers. The study revealed that although the wrestlers have enormous bellies, most of their abdominal fat is stored immediately under the skin, and not behind the stomach wall within the gut or visceral area. In fact, sumo wrestlers had about half of the visceral fat of regular people with visceral obesity.

This fat distribution is crucial to understanding body fat and health. While sumo wrestlers are not what comes to mind when we think of fit athletes, their training routines are quite intense. In fact, sumo wrestlers are only protected from health risks so long as they continue their intense training. When sumo wrestlers retire and veer away from their exercise program, they almost immediately develop more visceral fat and the classic problems of obesity such as high levels of insulin, insulin resistance, and diabetes.

Evidently, the sumo’s physical exercise and diet low in sugar helps him to avoid visceral fat. So how can strenuous activity prevent sumo wrestlers from getting obesity-related ailments?

Exercise has been shown to increase adiponectin levels. This hormone sensitizes the body’s response to insulin, and guides glucose and fat molecules out of our bloodstream and into body fat, where they belong. This is important because an excess of circulating glucose and fats in the blood are precursors for diabetes and metabolic disease. It also removes from circulation toxic lipids known as ceramides, which contribute to insulin resistance, inflammation, and cell death!

The sumo’s intense physical regimen (and the release of adiponectin) enables fat to be stored in the periphery instead of in the visceral area. And when the sumo curtails this exercise regimen, unhealthy visceral fat quickly accumulates.

The tale of the sumo wrestler is just one of many that I write about in The Secret Life of Fat showing the complex interactions that occur in our bodies which are rarely covered in one-size-fits-all diet books. Whether you’re looking to lose weight or learn more about one of the bodies most mysterious organs, follow along as I expose fat!