Sadly, there are no “secret” approaches for building a better body. However, with even a basic understanding of human physiology you can figure out a pretty rock solid plan to keep the pounds away. Of course, this presupposes you have long since given up the charade of fat loss being a math equation (calories in = calories out) and accepted that excess body fat is predominantly a biochemistry/hormonal problem.

This guy knows a thing or two about weight loss

Once you accept that in order to create sustainable fat loss, you have to manipulate metabolism, diet and hormones to create the proper internal environment, you have a fighting chance of being successful with your body transformation efforts.

When I work with a new client, I like to tell them that weight loss requires a multi-factorial approach. In other words, to have success we have to address:

1. diet
2. exercise/physical activity
3. recovery

Most people have an appreciation that losing fat will require adjustments to diet and exercise, but very few understand how important proper recovery is in all this. So today I thought I’d write about the forgotten fat buster: sleep.

Yeah, yeah, yeah… everyone knows they should get more sleep. But I bet you didn’t realize how stupid skipping sleep is if you are serious about positively transforming your body.

Let’s imagine you a busy individual who only sleeps 4-5 hours a night. Any idea of what that can do to your hormones? Thankfully I do and I’m going to share it with you right now! Below are the results of a neat little study that looked into the hormone changes (leptin and ghrelin) that are produced by just 2 consecutive nights of limited sleep:

• When leptin decreases: you experience a decrease in metabolic rate and increase appetite.
• When ghrelin increases: you experience increased hunger and appetite.

Wow… knowing that, those numbers look even worse than before! As you can clearly see, even a couple of nights of shoddy sleep will send our hunger control hormones (leptin and ghrelin) out of control!

Now imagine the real-world significance of these hormonal changes. If you were to act on a 30% increase in appetite for high carbohydrate foods, you might find yourself mowing down on a 300-400 kcal muffin or bagel, which would send insulin levels skyrocketing then plummeting, then a vicious cycle of hunger would begin…

See where I am going with this?

Making matters worse, if you only sleep for 4 hours, you’ve got a whole 20 hours to fall prey to those cravings. Needless to say, if you are not making sleep a priority, then you are seriously jeopardizing your body composition efforts.

Here’s some “secret” weight loss advice: turn off the television, email or your Blackberry and get to bed at a reasonable hour. It doesn’t cost you anything that the long-term benefits are priceless.

Seriously – you aren’t that important.

Just something to think for anyone looking for the “magic pill” that will cure your weight loss woes.

Till next time, train hard and eat clean!

In part one of this series, I discussed how universal truths are a standard bit of rhetoric in the fitness industry. In part two, I offered some reasons for how the scientific literature has unwittingly supported this naïve view. Then in the latest installment, I pointed out how more enlightened practitioners have attempted to classify individuals based on somatotype, in order to better define an individual’s dietary needs.

Unfortunately, although the somatotype categorization is a quantum leap forward in establishing dietary recommendations (in my opinion), it doesn’t always work quite so perfectly in the real-world.

Why Can’t Life Be Simple?

Recall that according to somatotype theory, a short, squat individual is labelled an endomorph. Correspondingly, they should consume a high protein, high fat, type of diet.

While this recommendation often produces excellent results, occasionally it doesn’t work very well at all.

Why might this be the case?

Only one way to find out… off to dig through some original research to see if we can locate the answer…

Although somatotyping has been around for ages, there is a surprising lack of research linking body fat distribution and diet recommendations. However, I was able to come up with a couple of studies that shed some light on the issue.

Insulin Sensitivity and Weight Loss Success

Back in 2005, researchers in Colorado took two groups of over-fat females (BMI: 30-35 kg/m²) and stratified them based on insulin sensitivity. Subjects were included in the study if they were insulin sensitive (IS), defined as having a fasting insulin level of < 10 µU/mL, or insulin resistant (IR), as determined by a fasting insulin level of >15 µU/mL.

The goal of the study was to compare weight-loss after 16 weeks of dieting (400 kcal deficit/day) on diets of differing macronutrient composition. The two diets under investigation were:

• HC/LF: 60% CHO, 20% fat, and 20% protein.
• LC/HF: 40% CHO, 40% fat, and 20% protein.

So in total this study had 4 conditions:

1. Insulin sensitive eating a high carb/low fat diet.
2. Insulin sensitive eating a low carb/high fat diet.
3. Insulin resistant eating a high carb/low fat diet.
4. Insulin resistant eating a low carb/high fat diet.

Still following me?

Good.

So after 16 weeks, what did these researchers report?

Obes Res. (2005). Insulin Sensitivity Determines the Effectiveness of Dietary Macronutrient Composition on
Weight Loss in Obese Women, Human Physiology, 13:703–709.

First the good news: every group lost weight. Now the even better news: by tailoring diet advice to an individual’s physiological responses, it may be possible to produce substantially greater weight loss!

Among individuals with good insulin sensitivity, weight loss was nearly twice as effective when following a higher-carbohydrate diet. As I’ve pointed out previously, having good insulin sensitivity is critical if you are going to consume a high carbohydrate diet.

But this data also suggests that not only is having good insulin sensitivity critical when consuming a high carbohydrate diet, but that individuals with good insulin sensitivity actually respond better (in terms of weight loss) eating more carbohydrates!

Conversely, individuals with poor insulin sensitivity (i.e. they were insulin resistant), lost far more weight when they consumed a diet higher in fat.

I suspect weight loss would have been even greater in the insulin resistant group had the researchers  selected an even lower carbohydrate level. However, in the interests of performing a well-controlled study, protein intake needed to be kept constant.

What this suggests is that if you have poor insulin regulation (partially a function of your genetics, but also potentially as a result of your lifestyle), you should NOT consume a diet high in carbohydrates.

Just a hunch, but I’m guessing this man does not have good insulin sensitivity…

Both of these outcomes make perfect sense when we look at the underlying physiology, yet somehow the need for personalized diet recommendations based upon an individual’s biochemical and physiological make-up still remains a foreign concept to many in the nutrition field… <sigh>, maybe one day.

GT’s note: this study is just one more piece of concrete evidence that weight-loss advice consisting solely of calorie counting is of limited use. Clearly, we must also consider specific endocrine and metabolic responses to particular foods.

All of this looks quite promising, so what’s the problem?

Taking Typing One Step Further

The problem with findings such as this one is that it points to somatotyping as overly simplistic. Remember, all the individuals in this study had BMIs over 30. This means that had we used anthropometrical or even visual data, we would have misclassified a number of individuals.

Although a somatotype-based diet recommendation may account for underlying physiology better than the alternative (one size fits all recommendations), it certainly isn’t fool proof.

Thankfully, we may be on the cusp of some major breakthroughs in our understanding of diet individualization!

Earlier this year, researchers out of Stanford University presented a re-analysis of data from the A to Z weight loss study that showed dramatically greater weight loss occurs when matching individuals to diets based on simple genetic markers.

Originally, the A to Z weight loss study was designed simply as a year-long comparison of the effectiveness of the Atkins (very low carb), Zone (40% carb, 30% protein, 30% fat), Ornish (very low fat, <10% of total calories) and LEARN (a lifestyle behaviour-change program) diets.

Much like any reasonable diet study, researchers randomly allocated their 311 overweight, premenopausal females subjects to one of the four diet conditions and tracked results over the 12-month time span.

At the study’s conclusion, the weight loss results were as follows:

• Atkins: -4.7 kg (95% confidence interval: -6.3 to -3.1 kg)
• Zone: -1.6 kg (-2.8 to -0.4 kg)
• LEARN: -2.6 kg (-3.8 to -1.3 kg)
• Ornish: -2.2 kg (-3.6 to -0.8 kg)

Had the researchers stopped their analysis right there, one could conclude that the Atkins diet is the best diet for weight loss, because that’s what the data suggests.

Fortunately, the researchers collected DNA swabs on 101 of these women. Tests were performed on these DNA samples and researchers were able to identify 3 distinct genotypes:

• a low carbohydrate diet responsive genotype (LCG, n=61)
• a low fat diet responsive genotype (LFG, n=35)
• a balanced diet responsive genotype (BDG, n=5)

When the data was re-analyzed with this concept of bio-individuality in mind (discussed in part 3 of this series), a very different story emerged.

Nelson MD, Prabhakar P, Kondragunta V, Kornman KS, Gardner C. Genetic Phenotypes Predict Weight Loss Success: The Right Diet Does Matter. (Oral Presentation #4). Presented at the American Heart Association’s Joint Conference – 50th Cardiovascular Disease Epidemiology and Prevention and Nutrition, Physical Activity and Metabolism – 2010, March 2-5, 2010, San Francisco, CA. Available online here.

When classified by correct vs. incorrect genotype, correctly matched individuals lost 2-3x more weight (~13.2 lbs vs. 4.6 lbs) than individuals who were placed in the wrong diet condition.

In other words, when an individual who is genetically predisposed to poor carbohydrate metabolism was placed on the low carbohydrate Atkins diet, they lost a ton of weight. A similar result was found when individuals with a strong carbohydrate metabolism were placed on the Ornish diet, they lost a lot of weight.

However, when an individual with a genetic predisposition for favourable carbohydrate metabolism was given the Atkins diet, results were predictably abysmal; same story occurred when individuals with poor carbohydrate metabolism were placed on the Ornish diet.

If you’d like to look over some of physiological rationale behind the genetic test used in this study: click here.

Once again, solid evidence that by correctly matching a diet to an individual’s biochemical make-up, demonstrably greater weight loss can be achieved.

Individualization in the Real World

Although this kind of research is exciting, we are still a good ways away from having easy, affordable access to these kinds of genetic tests.

We also need more research to verify whether the population breakdown of 60% low-carb genotypes, 35% high-carb genotype and 5% balanced genotype is one that holds true for the North American population as a whole, or whether it was unique to this study.

Regardless, results such as these definitely support the efforts that practitioners have made to stratify people by diet type.

At the current time, no one can say for certain whether the optimal breakdown will ultimately involve 3, 4, 6 or even 12 different metabolic types; however, it’s abundantly clear our answer is NOT “one size fits all”!

Of course, identifying what an individual should eat is only half the battle, convincing them to change their dietary habits is an entirely different challenge.

In the final installment of this series, I’ll let everyone try a tool that I’ve had success using to help match individuals to an optimal diet approach.

Stay tuned for that!

Till next time, train hard and eat clean!

Our national holiday marks the unofficial start to our all-too-brief summer season and what is more quintessential Canadian summer than rushing outside to soak up some rays?

But before you run off to the beach or up to the cottage, you mustn’t forget about protecting yourself from the sun, right? I mean, that’s the message we’ve had drilled into our collective psyches over the past 30 years, often through the use of creative ad campaigns.

Take Australia’s sun protection message that began in 1981: Slip-Slop-Slap. This campaign, which counsels people to “slip on a shirt, slop on sunscreen, and slap on a hat”, has been heralded as both ingenious and necessary, given that Australia has one of the highest rates of skin cancer in the world.

Click here to view the embedded video.

Clearly, governments around the world have decided there’s tremendous value in promoting the message: too much sun exposure = skin cancer.

Given how diligent we, as Canadians, seem to be about applying sun screen before any outdoor activities, it appears as though we’ve received the “protect yourself from sun message” loud and clear… only one small problem: this message is in stark contrast to the data.

Don’t believe me? Take a look for yourself…

Remember when I mentioned that Australia started their Slip-Slop-Slap campaign in 1981? Well shortly after launching their sunscreen campaign, look at what happened to their skin cancer rates:

These data slides are taken from a presentation done by Ed Gorham and colleague from the Faculty of Family and Preventatitve Medicine at the University of California, San Diego. The following data slides come from their presentation on vitamin D, skin cancer and sunscreen (accessible at: Skin Cancer Sunscreen Dilemna).

Yowsa. That’s a pretty dramatic increase in skin cancer incidence. But one could argue these results are an aberration. Let’s see what other data is out there.

Off to the US where Connecticut, amazingly, has maintained a tumor registry ever since the 1930′s. Why they have such detailed records is beyond me, but I’m not complaining; it makes for a great analysis of historical trends. What do we see there?

Seems that up until about 50 years ago, synthetic sun screens of any kind were non-existent, as were skin cancer rates. Then in Connecticut, like in Australia, there is quite the damning evidence that once sunscreen use became more prevalent, skin cancer rates also rose dramatically. This is not good.

However, before we get too crazy, let’s acknowledge that this data is correlational. I suppose these relationships could be mere happenstance… except when you start to include controlled studies, you get a similar story.

Wow. At best, these data suggest that sun screen doesn’t work. At worst, they suggest that using sunscreen slightly increases your risk of developing skin cancer. Just what the heck is going on!?!?

Let’s consider the human-sun relationship logically for a second. Up until relatively recently on the evolutionary time-scale, humans were exposed to the sun’s rays pretty much 365 days a year without the benefit of sunscreen. We simply wouldn’t have been able to survive in cold climates, therefore we would have migrated to live in relatively warm climates with plenty of sun exposure.

But did our ancestors routinely die of skin cancer while living in warmer climates? Impossible to say, however, we need not only delve into historical speculation. We can actually test the sun exposure = skin cancer hypothesis today.

If sun exposure = skin cancer, if would be reasonable to expect that skin cancer rates would be highest in those areas of the world hovering around the equator, as they get sunshine year-round.

But when we look at these data, tell me what you see:

Data obtained from the Cancer Research UK website

It certainly doesn’t appear that people living in sunny areas of the world are particularly predisposed to developing skin cancer. Nor is it a slam-dunk argument that only fair skinned individuals get skin cancer, as Eastern Europeans and the Japanese are both quite fair skinned, yet exhibit low rates of skin cancer.

If anything, it seems as though nations that get less sun exposure, or whose vocations tend to be indoors, rather than outdoors seem to be at greater risk for developing skin cancer.

Hmmm… could it be that the fact that humans managed to co-exist with ample sunlight for millennia upon millennia without any problems should tell us something? Might routine sun exposure actually be health promoting? Might our recommendations for sun avoidance be grounded in folly?

If you answered yes, yes and yes, pat yourself on the back. The reason why sun avoidance and an over-prescription of sunscreen makes zero sense has to do with vitamin D production.

Our uncovered skin produces vitamin D following sun exposure. Specifically, our skin produces vitamin D after exposure to UVB light (the wavelength most prevalent between 10 AM and 2 PM). In as little as 20 minutes of UVB sun exposure, a human will produce anywhere from 10,000-20,000 IU of vitamin D.

I know our current recommendation for vitamin D is only 400 IU per day and that you fear producing 20,000 IU of vitamin D might cause you to overdose. I mean, who hasn’t heard that fat soluble vitamins, like vitamin D, are potentially toxic? That the sun’s rays between 10 AM and 2 PM are the most “deadly”? Thankfully, the reality is that you’ve got nothing to fear.

In theory humans can overdose on vitamin D supplements, but one lovely fact about our physiology is that we shut off vitamin D production once we reach an optimal level. Our bodies are pretty smart like that.

Well realizing that our bodies have evolved a mechanism of producing a critical nutrient from the sun and a natural mechanism to cease production when we have enough is certainly comforting. But what about the recommendations saying we only need 400 IU of vitamin D per day?

Turns out that that amount of vitamin D is enough to prevent rickets, but nowhere near the amount needed to optimize your immune system and hormone regulation as a whole.

Now I’ll be the first to caution anyone against deliberately cooking themselves to the point of getting a sunburn. However, even a mild sunscreen, SPF 8, will block over 90% of our vitamin D production.

For a northern nation where UVB sunlight is virtually non-existent from October through April, limiting our already brief window of natural vitamin D production doesn’t seem like all that smart of an idea.

Good Canadian… bad science

But what exactly does vitamin D do for us?

Vitamin D is actually a group of fat-soluble secosteroid hormones. Given that it is a hormone, vitamin D has a wide range of effects on the human system. Among the systems or conditions that benefit from vitamin D are:

• immune system function
• influenza protection
• heart disease
• stroke
• hypertension
• autoimmune diseases
• diabetes
• depression
• chronic pain
• osteoarthritis
• osteoporosis
• muscle weakness & muscle wasting
• birth defects
• periodontal disease
• and 17 types of cancer!

Phew. That list is quite extensive isn’t it? If you said that vitamin D positively affects every single meaningful healh condition currently affecting humankind, you probably wouldn’t be too far off the truth.

Obviously I’m going to draw your attention to the last point, that increasing vitamin D production protects against 17 types of cancer. Even if we could conclusively prove that excess sun exposure caused skin cancers (and from the data above, it doesn’t really appear that way), does it make a whole lot of sense to increase your risk for all of the above disorders in order to protect yourself from one of the most treatable forms of cancer?

Recently, Dr. Mike Eades (a bariatric doc and someone with a strong appreciation for evidence-based medicine) wrote a couple of brilliant articles about sun exposure and cancer rates. If you’ve got 5 minutes, I strongly recommend you check his most recent post: Heliophobe Madness.

Among the many valuable points he makes, is a stunning comparison between the mortality from skin cancer vs. breast, colon and prostate cancers, three cancers that are linked to a deficiency of vitamin D. He quotes data from the American Cancer Society which reports that in the US in 2009, 40,230 people died from breast cancer, 32,050 from prostate cancer and 51,370 from colon cancer. That makes 123,650 individuals who died from these cancers combined.

By contrast, 8,700 US individuals people died from skin cancer. So even if sun exposure leads to skin cancer, we are pushing an intervention, massive sun screening, to protect against one of the mildest and most treatable forms of cancer, in exchange of increasing people’s risk of developing far more deadly forms of cancer.

Makes sense to me… or not.

Since this post has already gone on forever, I’ll wrap it up here. But if you are interested in learning more about vitamin D and the misguided science behind sunscreens, I suggest you check out this short video:

Click here to view the embedded video.

If you’ve got an interest in learning more about this important topic, I urge you to check out Ed Gorham’s excellent presenation on vitamin D production, sun exposure and sun screens:

Click here to view the embedded video.

Alright now… go enjoy yourself some of the health promoting UVB sunshine. Just don’t try to get an entire summer’s worth of sun exposure in a day

Till next time, train hard and eat clean.

Whenever you eat foods that provokes a substantial insulin release from your pancreas, your body is signaled to build either fat,  muscle or both. Obviously, the more structured resistance training you follow and the better you time your insulin spikes, the better able you are to use insulin’s mass building effects for muscle growth and not fat. Sadly, the common eating pattern in North America is to eat insulin producing foods without much foresight, which is part of the reason we battle the bulge.

Wild swings in insulin also tend to provoke increased hunger, which is not good if you are trying to control intake and by extension, body weight. I think it goes without saying that teaching people how to avoid crazy swings in insulin is a good thing.

In the 1980′s, David Jenkins from The University of Toronto, was the first to quantify how quickly food is digested and raises blood sugar. His system became known as the glycemic index (GI).

The creation of the glycemic index was a quantum leap forward in highlighting how seemingly similar foods can have wildly different biochemical properties in our bodies. In fact, the GI was such a popular and powerful idea that it spawned an entire series of diet books and programs, books that still can be found in bookstores today.

Unfortunately, subsequent research has shown us that are several major problems with basing food choices solely off the glycemic index. One of the major problems is that the glycemic index was derived studying foods in isolation. In reality, we typically eat mix-meals which throws off the GI readings.

Additionally, the method of food preparation and cooking can change the GI of a particular food. I spoke at a conference recently and one of my fellow presenters, Dr. Lonnie Lowery,  delivered an excellent talk on food preparation. He pointed out that if you freeze, then toast, white bread you can dramatically lower its GI. Keep in mind I still don’t think this makes white bread a particularly healthy choice, but it’s still neat to see how cooking can change the properties of our foods.

However, the biggest shortcoming of the GI is that it does not account for typical serving sizes. You see, in order to standardize the measure, the glycemic index is based on a representative serving size of 50 grams of the food in question. Sadly, this has caused some high glycemic index foods (i.e. carrots, watermelon) that aren’t typically eaten in 50 gram quantities, to still struggle to shed their “foods to avoid” label anti-GI zealots.

To address this shortcoming, later research suggested the concept of glycemic load (GL), which is just a function of the GI of a particular food x typical serving size.

As we can see in the table below, many of the moderate/high glycemic index vegetables and fruits actually have a low glycemic load, whereas most cereals and grains (with the exception of high fiber cereals like All Bran), have quite a bit higher glycemic load.

Perfect. For anyone wanting to avoid insulin surges and control body fat it’s case closed, right? Just eat low glycemic load foods…

Errr, not exactly.

It turns out that although glycemic load is highly correlated to insulin release, there are several low glycemic foods that can cause remarkably high insulin surges. These foods may or may not need to be avoided by insulin resistant individuals who are trying control body fat.

Insulin Index (downloadable sheet)

As you can see, most foods that are high GI foods also rank quite highly on the insulin index, but a couple of foods stand out for disproportionate insulin release: milk products, beef, fish.

But how is this possible? Well milk and most milk products contain a lot of sugar, so it makes sense why their insulin index would be higher and be contraindicated for insulin resistant individuals; but beef and fish? They contain zero carbohydrate, so what gives?

Even though carbohydrates are the major macronutrient from an insulin perspective, certain amino acids are capable of provoking an insulin surge as well. Take the branch chain amino acid leucine for example.

Leucine is particularly good at signaling “growth” of new muscle. Following a large protein meal when circulating leucine would be high, insulin is released to help pull amino acids from the blood into the muscle, stimulating new muscle growth.

By contrast, an insulin surge provoked by excess sugars will pull carbohydrates into the muscle. But when muscle glycogen levels are full, the excess sugar must be converted into body fat.

A day’s workout for the average Joe

Considering most of us aren’t terribly active on a daily basis, we have near maximal glycogen levels 24/7, as a result any excess sugar consumption tends to be quite detrimental.

Furthermore, unlike carbohydrates, purely protein foods not only result in increased insulin, but also cause your body to secrete glucagon. Glucanon is a hormone that opposes some of the potentially harmful effects of insulin. As a result, although high protein foods can cause a significant insulin release, they rarely have the same blood sugar crashing, hunger-inducing properties that high carbohydrate foods do.

Which means: better hunger control in the long run!

Therefore, despite the promise of classifying foods based on a single index, once again we are faced with an index that can at best be labelled “incomplete”.

Does this mean that all food indexes are destined for failure? Not necessarily.

In fact, the same researchers who developed the insulin index (Sue Holt and colleagues out of The University of Sydney), also did some work on a satiety index. Satiety, for those of you unfamiliar with the term, is a term used indicate how well a food satisfies a person’s hunger.

In my opinion, discovering what foods work best to nullify hunger is way more important in terms of real-world results than figuring out which foods cause the biggest boost in either blood sugar or insulin. But that’s just me and my somewhat bizarre belief that we need to value real world outcomes over results produced in a test tube or research lab… I know, I’m weird like that.

I’m only going to throw up a small version but you’ll get the idea. All the scores are based on a 240 kcal serving referenced back to white bread:

As you can see, even high glycemic foods like oatmeal and unprocessed potato do a great job of killing people’s hunger. Whereas certain foods promoted by dietitans everywhere as good weight loss foods (i.e. yogourt) do a pretty terrible job promoting satiety.

This is why I recommend oatmeal (and things like quinoa), potatoes and sweet potatoes be the starchy carbohydrates of choice for anyone serious about their health and body composition.

Not only do they contain less junk than breads, pastries and cereals, but they do a far better job helping control your hunger. Note, this still doesn’t give you carte blanche to eat oatmeal all day long, but opting for a filling, nutritious carbohydrate when your meal plan calls for carbs is just the smart choice in my books.

If I’ve said it once, I’ve said it 1000 times: if you control someone’s hunger, you’ll control their body weight over the lifespan.

So the next time someone comes to you preaching about the latest, greatest way to “judge” a food’s worthiness, ask them a simple question: “but will it help control my hunger?” If the answer is no, then odds are it’s not going to help you build a better physique over the long haul.

Till next time, train hard and eat clean!

Fat Head

Regardless of whether you are a low-carber or not, taking a few minutes to watch this video will serve you well:

Click here to view the embedded video.

I love this video because it provides a nice, easy to understand summary of how insulin controls blood sugar and by extension, body fat. Admittedly, the hormonal interplay that governs body fat regulation is infinitely more complicated than what the video suggests, however, insulin is definitely one of the key players in the creation of excess body fat.

The video also helps us see why proper insulin management is central to any diet. Although some lucky individuals have such a great innate tolerance for carbohydrates that they can, and must, eat a large percentage of total calories as carbohydrates; the majority of us must regulate our insulin through the diet and exercise.

Another aspect of this video I love is the suggestion that people don’t necessarily get fat because they eat too much. Rather, people eat too much because they are fat. This an incredibly powerful idea and one that helps explain why so many of our current diet theories fail miserably.

Basically, we continue to treat obesity all wrong. We need to let go of the belief that fat is just a storehouse of calories and instead accept fat as a metabolically active endocrine tissue. Only once we accept the role fat plays in endocrine dysfunction, will be be able to remove elements from the environment that negatively impact our hormonal status.

I know delving into the nutritional science can be daunting for the uninitiated, however, Gary Taubes is quite an accomplished science writer who has penned a number of brilliant essays. Here are two pieces of work that are a great place to start:

1. What if It’s All Been a Big Fat Lie?
2. The Soft Science of Dietary Fat

I’ll be back next week with a look at some of the fat producing hormones in greater detail. Until then, train hard and eat clean!