Category Archives: insulin

Top five reasons why you should remove grains from your diet for good

by Eric Hunter 

(NaturalNews) Government guidelines and advice from medical doctors can often lead people to believe that cereal grains are the foundation of a healthy diet. The food pyramid, now renamed the food plate, dictates that people should eat several servings of whole grains each day to provide an adequate supply of vitamins, minerals and fiber. This advice is given despite the fact that humans are poorly adapted to the consumption of cereal grains and that the scientific literature shows that grain consumption is linked to several health problems.

Grains have only been a part of the human diet for about 10,000 years, which is a very small time in the context of evolution. Just because humans can tolerate grains to a certain degree doesn’t mean that we are designed to consume grains or that we can achieve optimal health on a grain-based diet.

1) High-carbohydrate density and increased insulin load

Carbohydrates are eventually converted into a simple form of sugar, glucose, after they are consumed. Insulin is secreted and allows glucose to be transported into various cells throughout the body. Individuals who aren’t very physically active don’t have the need to continually refill their muscle and liver cells with glycogen, and these cells often start to become insulin-resistant on a grain-based diet.

Regular consumption of high-density carbohydrates is not only linked to insulin resistance and overweight, but also leptin resistance, altered gut flora and inflammation.

2) Antinutrients

Grains are the reproductive material of the plant, and plants don’t make the reproductive material to give away for free to animals. Cereal grains have evolved Lectins, Phytic Acid, Protease Inhibitors and other anti-nutrients that potentially disrupt normal gut physiology when they are consumed over time. Only certain anti-nutrients are problematic in humans, and they seem to operate in a dose-dependent manner.

Regular consumption of anti-nutrients in grains may lead to poor mineral absorption, autoimmune disease, leaky gut and low-level chronic inflammation. More studies on human subjects are needed to fully understand the detrimental effects of Lectins and other anti-nutrients on human health.

3) Gluten

Studies and anecdotal reports indicate that gluten intolerance is much more common than previously thought, and many asymptomatic individuals react to gluten with some type of inflammatory response.

4) Insoluble fiber

While fruits and vegetables contain heart-healthy, soluble fiber that promote good gut flora, cereal grains are high in insoluble fiber that shouldn’t be eaten in excess. More insoluble fiber is often recommended for healthy digestion, despite the fact that healthy gut bacteria is the key to relieve constipation and achieve healthy bowel movements.

5) Dietary imbalances

Cereal grains have several dietary shortcomings, and a grain-based diet can disrupt adequate nutritional balance. Cereal grains are poor sources of fiber, minerals, vitamins and protein compared to animal products, fruits and vegetables. They contain no vitamin A, vitamin C, vitamin B12, calcium nor sodium, and several animal studies show that grain consumption can induce vitamin D deficiencies and alter the metabolism of several minerals.

Cereal grains only supply some of the essential amino acids, very few essential fatty acids and are also characterized by a high omega-6 to omega-3 ratio.

Traditional grain preparation
Some traditional cultures have been known to consume grains on a regular basis and still maintain excellent health. However, these populations have usually used soaking, sprouting and fermentation to make the grains easier to digest. These preparation methods remove or deactivate some of the anti-nutrients commonly found in grains, and fermentation is especially effective when trying to make grains more digestible.

Sources for this article

Cordain L. Cereal Grains: Humanity’s Double-Edged Sword
World Rev Nutr Diet. 1999;84:19-73.

Freed DL. Do dietary lectins cause disease?
BMJ. 1999 Apr 17;318(7190):1023-4.

Miyake K, Tanaka T, McNeil PL. Disruption-Induced Mucus Secretion: Repair and Protection
PLoS Biol. 2006 Sep;4(9):e276.

Dalla Pellegrina C, Perbellini O, et al. Effects of wheat germ agglutinin on human gastrointestinal epithelium: insights from an experimental model of immune/epithelial cell interaction.
Toxicol Appl Pharmacol. 2009 Jun 1;237(2):146-53. Epub 2009 Mar 28.

Biesiekierski JR, Newnham ED, Irving PM, et al. Gluten Causes Gastrointestinal Symptoms in Subjects Without Celiac Disease: A Double-Blind Randomized Placebo-Controlled Trial
Am J Gastroenterol. 2011 Mar;106(3):508-14; quiz 515. Epub 2011 Jan 11.

Drago S, El Asmar R, Di Pierro M, et al. Gliadin, zonulin and gut permeability: Effects on celiac and non-celiac intestinal mucosa and intestinal cell lines.
Scand J Gastroenterol. 2006 Apr;41(4):408-19.

About the author:
Eric is the editor of and a writer for He’s an independent writer with a strong interest in personal health and the power of nature to help us heal. 
He studies Public Nutrition and specializes in the human microbiome, inflammation and gut permeability.
Eric works as a personal trainer and currently coaches a few dedicated clients on their way to a better physique. He specializes on barbell- , kettlebell- and sprint- training. Subjects like mass building and weight loss are some of his favorites.
Eric believes that lifestyle choices have to be made on an evolutionary basis!

30 Seconds to Leanness

Sprinting for Leanness
by Mike T Nelson – 6/12/2012

Every time you turn around, there’s a new diet plan based on a hormone. While there’s some merit to all this madness, most of the plans fail to completely understand their respective physiological underpinnings. The body isn’t a simple, linear, straightforward machine – it’s complex and redundant at almost every turn.

This article will reveal some new research on the hormone leptin to provide some simple actions for you to take to help you get leaner. Just because the physiology is messy doesn’t mean your actions need to be complicated!

First, here’s a short crash course on this important hormone.

Leptin 101

Leptin was discovered by Ingalls and friends in the early 1950’s (Ingalls, AM, et al 1950). Fast forward to the early 90’s when it was “rediscovered”, and many were predicting it would be the biggest weight loss breakthrough ever.

It’s a hormone that is released primarily by fat cells (adipocytes) and works to regulate appetite, body fat mass, and basal metabolic rate.

Until just a few years ago, researchers thought that fat cells sat on their collective butts all day and were only a storage place for unsightly body fat.

We know now that those pesky fat cells are very metabolically active, releasing and receiving a myriad of messenger hormones, one of which is leptin.

How Does Leptin Work?

Sprinting for Leanness
Leptin travels up to the brain where it acts on receptors in the hypothalamus to inhibit appetite.

More leptin in your brain = less food intake.

This is great news for anyone looking to get leaner, since more leptin means you’ll be less likely to prowl your kitchen at 3 AM in search of leftover birthday cake. Leptin is your body’s way of putting the brakes on fat gain by decreasing appetite.

The chronic level of leptin you have is also a rough measure of the amount of fat you have on your body. Many things can affect leptin as shown in the table below:

Factors promoting leptin secretion

Excess energy stored as fat (obesity)
Inflammatory cytokines, including tumor necrosis factor and Interleukin-6 (acute effect)
Factors inhibiting leptin secretion

Low energy states with decreased fat stores (leanness)
Catecholamines and adrenergic agonists
Thyroid hormones
Peroxisome proliferator–activated receptor-agonists
Inflammatory cytokines, including tumor necrosis factor (prolonged effect)

Leptin Super Mouse to the Rescue!

Researchers lead by Zhang,Y in the mid-1990s did a series of mouse experiments to show that mice with messed up leptin (ob/ob mouse) became fat little fury bastards (Zhang, Y et al. 1994).

Their metabolic rate was lower, they didn’t move as much, and they ate tons of mouse chow.

The catch was that this mouse ob/ob (think double obese) didn’t make any leptin at all.

To make the mouse lean, they injected it with leptin, and voila – a thin mouse again!

The researchers all joined hands, sang Kumbaya, and went out for tasty adult beverages while taking turns patting each other on the back for single-handedly solving the obesity problems. We just need to inject humans with leptin and poof, thin humans, and more visually appealing shopping experiences at Walmart.

The problem was it didn’t work.

Researchers measured blood levels of leptin in obese humans and found that leptin levels were sky high!

That wasn’t supposed to happen. Leptin levels were expected to be low since the humans were fat. As leptin increases, it signals that the body has enough fat, so we would expect low leptin levels in obese populations.

As you recall, when injected with leptin (thus increasing the level), the mice in the studies got thinner.

But these obese humans already had high levels of leptin. Injecting more leptin was like pissing in the ocean to try to raise the water level.

Leptin 201: The Receptor

It appeared that the receptor for leptin is out of joint. The receptor isn’t telling the brain that leptin is high. Tons of leptin, but the silly brain can’t tell since the receptor is as broke as Terrell Owens.

Why it Matters

Sprinting for Leanness

We already know that sprint training is a great way to burn fat, but it may have another benefit.

A study done by Guerra et al. in 2011 looked at sprints as a leptin signaling mimetic.

Unlike most research, this study used a group of T Nation style humans who were pretty lean (about 15% body fat) and young (23 years old). They split them into two groups: a fasting group, and a glucose group where they ingested 75 grams of glucose one hour before sprints.

Both groups did one Wingate bike sprint for only 30 seconds.

If you’re not familiar with this set up, in short, it’s hop on a bike set to a high workload (10% of body weight used here) and pedal like a rabid grizzly bear is chasing you.

What They Found

Subjects had a series of muscle biopsies done over the course of the study and researchers found that a single session of sprint training showed alterations in leptin signaling. The sprints were jacking up leptin that, in theory, should get the waddling Walmart shoppers to start dropping fat.

However, this was not seen in the group that ingested glucose before their sprint. Only the fasted group saw leptin alterations.

It appears insulin may interfere with the leptin signaling to some degree. To quote the researchers directly:

“Altogether, these results indicate that sprint exercise performed under fasting conditions elicits signaling events similar to those described in the rodent skeletal muscle after leptin injections, i.e. sprint exercise under fasting conditions acts as a leptin signaling mimetic in human muscle. However, glucose ingestion before the sprint training exercise blunts this effect.” (Guerra et al. 2011)

So it appears that fasted sprint training can pinch hit for leptin.

Do This! A Training Template

Sprinting for Leanness
Hop on a bike and work up to one maximum, all out, pedal-as-hard-as-you-can sprint for 30 seconds.

The tension should be relatively high, but the goal is to keep your pedaling at a fast pace for the entire 30 seconds. If you slowed to a snail pace 20 seconds in, go to a lighter workload.

Make sure this is done in a fasted condition, such as first thing in the morning.

Don’t have a bike? While the study didn’t look at running, it may elicit the same response as the pathways are very similar.

It sounds ridiculously simple, but my purely anecdotal experience with my athletes shows that this does seem to help speed fat loss.


More leptin is associated with less food intake.
Some may have a leptin receptor issue where it’s not responding to the amount of leptin floating around. Unfortunately, science isn’t at the point yet where we can easily tell who has a receptor issue, but the more overweight you are, the more prone you are to having broken leptin receptors.
Doing just one sprint in a fasted state works to pinch hit for leptin, putting you on the road to leanness. However, non-fasted training does not have the same effect. So add some sprint training in, but it has to be done in a fasted state.
Fasted sprints can be done any time on a fasting day (where you’re not consuming any calories), or done before breakfast. This way it’s unlikely to interfere with your normal training session.
While we don’t have a long-term study to show how much this will help your body composition, it’s simple to add in and there’s some very strong data to show it will help.
Sprinting for Leanness
Heck, it only takes literally 30 seconds to do the sprint. Try it out, and let me know what you find.

Questions or comments? Post them in the LiveSpill below.

Selected References

Everard, A., Lazarevic, V., Derrien, M., Girard, M., Muccioli, G. G., Neyrinck, A. M., Cani, P. D. (2011). Responses of gut microbiota and glucose and lipid metabolism to prebiotics in genetic obese and diet-induced leptin-resistant mice. Diabetes, 60(11), 2775-2786. doi:10.2337/db11-0227

Finocchietto PV, Holod S, Barreyro F, Peralta JG, Alippe Y, Giovambattista A, Carreras MC, Poderoso JJ. Defective leptin-AMP-dependent kinase pathway induces nitric oxide release and contributes to mitochondrial dysfunction and obesity in ob/ob mice. Antioxid Redox Signal. 2011 Nov 1;15(9):2395-406. Epub 2011 Jun 28.

Galgani, J. E., Greenway, F. L., Caglayan, S., Wong, M. L., Licinio, J., & Ravussin, E. (2010). Leptin replacement prevents weight loss-induced metabolic adaptation in congenital leptin-deficient patients. The Journal of Clinical Endocrinology and Metabolism, 95(2), 851-855. doi:10.1210/jc.2009-1739

Guerra, B., Olmedillas, H., Guadalupe-Grau, A., Ponce-Gonzalez, J. G., Morales-Alamo, D., Fuentes, T., . . . Calbet, J. A. (2011). Is sprint exercise a leptin signaling mimetic in human skeletal muscle? Journal of Applied Physiology (Bethesda, Md.: 1985), 111(3), 715-725. doi:10.1152/japplphysiol.00805.2010

Ho, J. N., Jang, J. Y., Yoon, H. G., Kim, Y., Kim, S., Jun, W., & Lee, J. (2012). Anti-obesity effect of a standardised ethanol extract from curcuma longa L. fermented with aspergillus oryzae in ob/ob mice and primary mouse adipocytes. Journal of the Science of Food and Agriculture, doi:10.1002/jsfa.5592; 10.1002/jsfa.5592

INGALLS, A. M., DICKIE, M. M., & SNELL, G. D. (1950). Obese, a new mutation in the house mouse. The Journal of Heredity, 41(12), 317-318.

Kelesidis, T., Kelesidis, I., Chou, S., & Mantzoros, C. S. (2010). Narrative review: The role of leptin in human physiology: Emerging clinical applications. Annals of Internal Medicine, 152(2), 93-100. doi:10.1059/0003-4819-152-2-201001190-00008

Kowalik, S., & Kedzierski, W. (2011). The effect of interval versus continuous exercise on plasma leptin and ghrelin concentration in young trotters. Polish Journal of Veterinary Sciences, 14(3), 373-378.

Plinta, R., Olszanecka-Glinianowicz, M., Drosdzol-Cop, A., Chudek, J., & Skrzypulec-Plinta, V. (2011). The effect of three-month pre-season preparatory period and short-term exercise on plasma leptin, adiponectin, visfatin and ghrelin levels in young female handball and basketball players. Journal of Endocrinological Investigation, doi:10.3275/8014

Wolsk, E., Mygind, H., Grondahl, T. S., Pedersen, B. K., & van Hall, G. (2011). The role of leptin in human lipid and glucose metabolism: The effects of acute recombinant human leptin infusion in young healthy males. The American Journal of Clinical Nutrition, 94(6), 1533-1544. doi:10.3945/ajcn.111.012260

Zhang, Y., Proenca, R., Maffei, M., Barone, M., Leopold, L., & Friedman, J. M. (1994). Positional cloning of the mouse obese gene and its human homologue. Nature, 372(6505), 425-432. doi:10.1038/372425a0

Do you need an insulin relief day?

Pulse Fast For Mass Phases

Bench Press

Pulse Fasting – Why Bother?

As soon as I heard about the Pulse Fast, my interest was piqued. The Pulse Fast was something aggressive that I could do just once per week, leaving the rest of my week alone.
Here’s the deal: I’m in the midst of a fall mass-building phase. I’ve already planned my diet very well. I’ve gained 16 pounds of lean mass since early summer. The Pulse Fast was something I could easily do once per week without changing the rest of my plan. 
So, perhaps ironically, I planned to “fast” during my bulking phase.

Insulin: The Jekyll and Hyde Hormone

I purposefully keep endogenous (internal) insulin flowing when gaining mass. But it’s been a while since I’ve done this, and I know insulin is a “Jekyll and Hyde” hormone – both friend and monstrous foe. Elevated insulin concentrations can help you build muscle or it can make you fat and lead to disease.
With chronically elevated insulin concentrations, particular genes get turned on and the fat-building machinery of cells gets overproduced, setting the stage for triacylglycerol creation and storage (fat gain).
Further, with my family history of Type II diabetes and obesity, I was aware that I may be a poor carb-handler, particularly now that I’m in my early 40s and no longer a multi-sport, hyperactive youth. Unwanted fat gain would be tougher to strip off in early spring.
I had to give my physiology a break from the past eight months of gain, gain, gain. I needed to re-train my body so the Hyde side of insulin didn’t begin to overpower the Jekyll side. In short, I needed insulin relief.
Still, I needed insulin on my muscles’ side, and in sufficient quantities to work with my other anabolic hormones. This is where Pulse Fasting came in.
By simply doing this augmented version of a protein-sparing modified fast (PSMF) once per week (when I’m crushed with work at the university and find it difficult to eat anyway) I could remove insulin’s presence to some extent and give my genetic machinery a break.

Insulin Relief: Not Gobbledygook

Okay, reality check. Genetic and cellular machinery? Temporal adjustments to hyperinsulinemia? Acetyl Co-A carboxylase?
Holy carboxylations, Batman, is this just all intellectual gobbledygook?
No, it isn’t.
A picture is worth a thousand words, so I thought I’d create one to illustrate to myself just how much “insulin relief” I’d be getting by employing a MAG-10 Pulse Fast one day out of seven.

Here it is:

Bench Press

Looking at the graph, you can see that moderately-sized casein and casein-plus-fat meals are mildly insulinogenic. Not quite at the magnitude of a 524 kcal mixed meal (19% protein, 63% carbohydrate, 18% fat) but that’s the point, isn’t it? As stated by Tipton (2004): “The magnitude of insulin response [to 20 g casein] was not great.”

The Right Magnitude of Change

Let’s consider peak insulin values across a day. The comment in the upper right of the graph shows that a pretty standard six meals for a grown man (about 3000 kcal per day) results in 400-500 units of peak insulin over six meals. That equals 2400-3000 total units secreted just at these peak times.
By contrast, the casein “pulse” values are clearly much lower. Even at 20-50 grams per dose or with 1g/kg of fat added, there’s not a whole lot happening. No carbs, less insulin. That’s pretty straightforward.
Multiplying-out the peak insulin values we get 65-79 units for ten pulses. That equals 650-790 total units secreted at peak times.
And it’s worth noting that Pulse Fasting is more along the lines of just 10g casein hydrolysate boluses – a smaller dose than 20-50g and that would lead to a somewhat smaller insulin response. On the other hand, MAG-10 is spiked with leucine, so we might be back up near 70 after all.
Leaving other issues to the side, this low and steady insulin effect puts my “Oh my God, I’m shrinking!” thoughts at ease, even as I take a day off of forced eating and start to retrain my biochemistry away from fat storage.

“Muscle-Sparing” vs. “Professor Pudge”

Another figure is called for to illustrate my thinking on “muscle-sparing” levels of insulin versus “Professor Pudge” levels of insulin:

If I’m theoretically producing roughly 75% less insulin one day per week, on that day my physiology reflects the lower half of the figure. That is, on Mondays I produce enough insulin to maintain muscle mass but not enough to keep my cellular machinery in fat storage mode.

The Final Verdict

A week-long computation suggests that I’m secreting 11 percent less insulin per week. That is, if I set my previous chowhound insulin levels as 100 percent max secretion for seven days, I’m now at just 25 percent output on Mondays, plus 100 percent on the other six days.
Eleven percent sounds perfect to me. It feels like the right magnitude of change at this point in my year-long macro-cycle. And this is just concerning the insulin side of the equation.  
Next time, I’ll ramble on about what else I see besides insulin underlying the MAG-10 Pulse Fast and I’ll offer some other thoughts, like what else a 40-something bodybuilder does to shift his physiology and mental state from mass-crazed off-season fork fiend to in-season lean freak.
Do you need an “insulin relief day” in your mass phase? Think about it. And let’s discuss below.


1. Keske M., et al. Obesity blunts microvascular recruitment in human forearm muscle after a mixed meal.Diabetes Care. 2009 Sep;32(9):1672-7.
2. Tipton, K., et al. Ingestion of casein and whey proteins result in muscle anabolism after resistance exercise. Med Sci Sports Exerc. 2004 Dec;36(12):2073-81.
3. Westphal, S., et al. Postprandial lipid and carbohydrate responses after the ingestion of a casein-enriched mixed meal. Am J Clin Nutr. 2004 Aug;80(2):284-90. 


Therapeutic Diet for Insulin Resistance

This low-carbohydrate, moderate-protein and moderate-fat diet is focused on real foods as the solution to Insulin Resistance Syndrome (IR), sometimes called Metabolic Syndrome or Syndrome X. It is mainly refined foods, especially sweets, combined with deficient exercise that gets people into trouble so a program based on whole foods, not more refined food products, is the best long-term solution in IR, and a host of other health problems as well. It is also recommended to take a good multiple vitamin/mineral.
Based on human evolutionary history and physiology this should be your most natural and optimal diet. It reflects what our Paleolithic ancestors (i.e., before agriculture) evolved eating over a million years and, as such, has the highest potential of supporting healing and preventing disease. In addition, this diet is naturally alkalizing, which is considered by some people to be healthier than the typical American acidifying diet. 
If you need more dietary support than this webpage provides, the popular diet that is closest to this IR diet is The South Beach Diet by Arthur Agatston, M.D. We also recommended reading The Paleo Diet by Loren Cordain, Ph.D. It gives a good background on the problems of the modern diet and the advantages of the Paleolithic diet. However, use this webpage as your main reference and refer to these books only for recipes, background and support.
It will take at least 2 to 3 months to reestablish normal insulin sensitivity. If there is severe IR or obesity it could take much longer to stabilize. However, most people will experience some improvements early on in the program. After stabilization has been shown through lab values, blood pressures, improved energy, loss of weight (especially abdominal), loss of carbohydrate cravings and loss of hypoglycemic symptoms, then switching to the Maintenance Diet for Insulin Resistance is possible. However, it will be essential to continue to monitor the lab values, signs, symptoms and weight.
With this diet you should not be hungry until its time for the next meal. If this is happening try increasing the non-starchy vegetables, nuts, fats and/or protein intake in the meals. Do not avoid naturally fatty foods, but limit saturated fats. Avoid hydrogenated oils and fried foods. For hypoglycemia symptoms eat smaller more frequent meals. Try to eat for hunger and not emotional reasons. If you must eat for emotional reasons, eat non-starchy vegetables or lean protein. Snacks should be non-starchy vegetables, nuts, seeds or protein foods.
PROBLEM CARBOHYDRATES (refined and starchy) – The cause of the problem!
·    No potatoes or simple sugars/carbohydrates (common table sugar, fructose, sweets, cookies, candy, ice cream, pastries, honey, fruit juice, soda pop, alcoholic beverages, etc.). Anything that tastes sweet (including artificial sweeteners and Stevia) may raise insulin levels, thus aggravating IR and perpetuating the cravings for sweets. As IR improves, sweet cravings usually decrease.
·    Almost no grain products (breads, pasta, cornbread, corn tortillas, crackers, popcorn, etc.) and no refined grains/carbohydrates (white flour products, white pasta, white rice, etc.).
·    Whole grains (whole brown rice, wheat, rye, barley and buckwheat) only in very small amounts.
GOOD CARBOHYDRATES (non-refined and non-starchy)
·    Small amounts of fruit are OK but eat it with protein meals and not alone. Berries are best. No dried fruit.
·    Eat lots and lots of non-starchy vegetables. Raw or lightly cooked is best. These should be the main source of carbohydrates in the diet. Fresh vegetables are best, frozen is OK but canned is to be avoided except for canned tomatoes and tomato sauce.
·   Legumes (beans, peas, peanuts, soybeans, soy products, etc.) have a low glycemic index so are OK.
·    Consume moderate amounts of leaner meats, seafood and fish. The best are wild fish, wild game, free-range chicken & turkey, range-fed beef, lamb, buffalo and naturally grown pork. Grain-fed means more saturated fats and omega-6 oils. Wild and range-fed means less of these and more omega-3s. The more omega-3s the better. Feeding grain to animals, like cows, that were meant to eat grass is not healthy for the animal nor the person eating the animal.
·    If you do not have a dairy allergy, some dairy is OK. Interestingly, the lower the fat in milk the more it raises the blood sugar, so low fat milk is worse than whole milk. But the best is no milk, it raises the blood sugar too much, plus cow’s milk is for calves, not people. Other dairy products are okay. Use only unsweetened yogurt. Limit butter and no hydrogenated margarine.
·    Eggs are fine unless you have allergies to them, but the best are eggs from free-range chickens and eggs grown to be high in omega-3 oils. Best is no more than 7 per week due to the high fat content.
·    For most people: moderate amounts of nuts (walnuts, macadamia nuts, almonds, cashews, pecans, etc.) and seeds (sesame, sunflower, pumpkin, etc.). Raw are best. Walnuts are high in omega-3s. Nut and seed butters are good (almond, cashew, sesame). Peanut butter and peanuts are legumes.
·    Consume moderate amounts of healthy oils. A low-fat diet is not healthy, nor is it compatible with this diet.
·    Healthy oils are: Monounsaturated oils (olive, canola, nuts). Polyunsaturated oils that are high in omega-3 oils (canola, flax, fish oils, walnuts). Saturated fats from vegetable sources (coconut, palm, avocado).
·    Limit animal sources of saturated fats as found in dairy products (cheese, butter, etc.) and most commercial red meats.
·    Freely add healthy oils to salads, sauces for vegetables and when cooking lean meats. Natural palm and coconut oil are excellent for cooking and frying. Flax oil is high in omega-3 oils but goes rancid very easily so refrigerate and do not heat and add only after cooking.
·    No hydrogenated oils and limit fried foods. Some low-heat frying with natural palm and coconut oil is okay.
·    Drink lots of pure water.
·    Organic is always best when available.
·    Cut down on salt but feel free to use other spices liberally.
·    Except for non-starchy vegetables, the other carbohydrates should be limited to protein meals.
·    It is usually safe to assume that most processed foods will interfere with this diet, even if low-carb.
·    Finally, it must be emphasized that exercise is a very important component of success.
Highly recommended vegetables.
Eat as many of these as possible for the best health.

Beet greens
Bok Choy
Brussel sprouts
Cabbage (green and red)
Chinese cabbage

Vegetables to use in moderation.
Collard greens
Dandelion greens
Lettuce (avoid iceberg)
Mustard greens

Vegetables to avoid.

Peppers(all kinds)
Swiss chard
Turnips greens


Three Hormones You MUST Address for Fast Fat Loss

It seems like most fat loss programs focus on one main thing: to burn fat, you have to expend more energy than you take in.
Such a focus makes sense, of course, because if there is a universal truth to fat loss, that’s it.
This is what we call “energy balance.”  In order to lose fat, you have to create what we call “energy debt” or “energy deficit” –that is, eliminate the balance and instead be on the negative side of the balance scales.
That works very well for “beginning” fat, of course.  However, success doesn’t last forever.
As anyone who’s ever been on a diet and exercise program of any kind can tell you, at first it’s pretty smooth sailing.  Eat less, do more, lose fat.
And then it stops—and usually, stops suddenly, as those same people can also tell you.
Of course, the first instinct people have is a very natural one: to simply do more of what was bringing them success in the first place. 
So they eat even less and do even more.
And…have no results.
You see, what these people fail to realize (and what most fat loss programs fail to address) is that:

After a certain point, simple energy deficit
no longer covers the tab.

It becomes more about what type of deficit. Speaking generally, you actually have to eat closer to maintenance calorie levels (instead of far below) and expend more Calories through exercise.
Even then, things don’t always happen as quickly as you want.
You see, once you’ve hit a fat loss plateau—or when you’re trying to lose the last few pounds, like I was when I was dieting for the beach house—fat loss becomes a bit less about energy balance a lot more about hormones.
Some hormones, such as leptin, actually control the majority of your general fat loss efforts and all the factors thereof: appetite, satiety, “starvation mode.” However, assuming you’re eating enough and trying to create an energy deficit through training, leptin isn’t the issue.
In Final Phase Fat Loss, you’re never on a severe diet, so you don’t have to worry about leptin.
There are other hormones which are a bit more insidious in their effects on your physique.  They don’t just determine IF you gain fat—they determine where you gain it, and whether you’re able to lose it from those areas.
Those “problem” areas on your body are there for a reason.
“Problem areas” are created by your hormonal environment, and it’s your hormones that force your body to have particular fat storage patterns.
In this article, we’re going to talk about the three most common types of regional fat storage, and the hormones that cause them.

Back Got Back: Low Body Fat Storage

One of the most common types of fat storage that we see in women is the “pear shape” –fairly thin on top but heavy on the bottom (and IN the bottom, if you know what I mean).
This is so common that we often refer to a “pear shape” as a body type.  This is true to an extent, but this type of fat storage is also heavily dependent on the female sex hormone estrogen.  This is one reason why you see this type of fat storage primarily in women.
High levels of estrogen are awesome for enjoying Grey’s Anatomy and makin’ babies, but terriblefor fat loss, which makes it obvious that women usually have more trouble losing fat than men.
However, anyone—male or female—with high estrogen levels will have trouble losing fat,especially from the lower body.   In essence, the higher your estrogen levels, the greater the likelihood you’ll store fat in your lower body; mainly in the hips and thighs.
And yes, it IS possible for men to have high estrogen levels.  Unfortunately, outside of having to deal with a declined rate of fat loss and lower body fat, these guys ALSO have to deal with the ignominy of man-boobs. 
On the whole, estrogen related fat storage is a pain in the ass (get it!?) but it is not completely unmanageable.  You see, you can offset this phenomenon with certain types of training. 
In addition to helping you lose fat stored in the lower body, these specifically designed workouts will also be great for fat loss in general.  Essentially, they’re great for burning calories and for shedding lower body fat through estrogen management—combine the two and the result is rapid fat loss, with a heavy concentration on lower body fat stores.
No worries, ladies (and gents!), I’m here to help.

Muffin Tops:  No Love for the Love Handles

Probably my least favorite incarnation of regional fat storage is love handle and lower back fat.  This is, of course, because I personally suffer from such.
Even when I am in lean condition—I’m talking shredded pretty much everywhere else—
I store some fat in my love handles and lower back.  It used to take me an extra 3 weeks to get rid of it.
The reason I tend to store fat this way is because of how my body reacts to certain hormones, and because of the effect those hormones have on fat storage.
When I was a fat kid and ate lots and lots of goodies, I screwed by my endocrine system a wee bit.  Nothing too serious, but a decade of eating rapidly digesting carbs followed by…well, followed by more rapidly digesting carbs made my insulin spike and crash and spike and crash all over the place.
On top of making me fat in that immediacy, it also completely had a pretty negative effect on the way my body processes and handles insulin period.
The degree to which you are able to process and respond to glucose (sugar) in your body is called insulin sensitivity.  The higher this is, the easier and more efficiently your body utilizes carbohydrates for energy, and the less like you are to store carbs as fat. 
On the other hand, insulin resistance is the opposite: you don’t deal well with carbs, and anything other than a low carb diet pretty much means you’re gonna hang on to some fat.
And, to make matters worse, as I mentioned previously, there are regional effects.  It’s been shown that people who store fat in the love handles are generally very insulin resistant—and therefore it can be reasoned that insulin resistance leads to love handle and lower back fat storage.
Which means, of course, that insulin resistance makes it very hard to lose fat from that area as well.
I’m sure many of you out there who have been heavy before are experiencing much the same problems that I used to have.
The good news is that insulin resistance (and the resulting regional fatness) can be mitigated with certain types of training.  For example, with careful planning and selection of exercises, you can start to whittle away at love handle and lower back fat while you increase insulin sensitivity. 
The better news is that I’ve figured out a specific series of training sessions that will do just that.

The One, The Only:  Belly Fat

Without question, the most common type of regional fat storage is belly fat. If this isn’t you, it’s someone you know. 
Abdominal fat storage obviously has a lot to do with your diet and overall body fat level; that should be obvious but it never hurts to touch on it.
Outside of that, it’s hormones baby, hormones. 
The one we’re talking about here is cortisol.  This hormone has been in the media a lot the past few years, and I’ve talked about it a bit, so by now you know that cortisol is sometimes called a “stress” hormone.
That moniker is more appropriate than you know.
Basically, that means your body will produce cortisol (and encourage belly fat storage) under conditions of nearly any type of stress—both emotionaland physical.  So to combat cortisol, it’s not enough to just get more sleep or stop drunk dialing your ex-girlfriend.  (Although that helps, I’ve heard.)
Instead, it is of far greater effect to combat cortisol through resistance training.
Now, if you’re observant, you may have noticed what seems to be a contradiction.
As I said, cortisol is also produced through physical stress.  In fact, training is actually one of the primary means through which your body will produce this sneaky little hormone.  Additionally, because cortisol has been linked to overtraining and has a catabolic (muscle wasting) effect, producing too much of it through training is certainly counterproductive.
It’s important to note, however, that long duration cardio and extended lifting sessions are what produce the most cortisol, and I always recommend against those.
Instead, short, intense training sessions using a particular type of training modality will help to counteract the effects of cortisol; both the muscle-wasting effect, and the cortisol related belly fat storage.
I’ll share that with you tomorrow.
In fact, tomorrow I’ll be sharing another entire article with you.  In that article, I’ll teach you how to fight hormones with hormones.  I’ll show you how to use specific types of training to combat the nefarious three hormonal nemeses by producing hormones that offset the effects of estrogen, insulin and cortisol.
Be on the look-out for “How to Conquer Your Hormonal Nemeses” tomorrow.  In the meantime, if you did not read The Final Phase Fat Loss “Origin” Story, make SURE you go do that right now by clicking HERE.  It’s the only reason Final Phase Fat Loss exists, and I can guarantee you’ll be able to relate to the exact position I was in (and overcame) when prepping for my own “big event”.
Keep going strong,

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