Category Archives: insulin
(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.
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.
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 include:
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 OrganicFitness.com and a writer for GutFlora.com/TheGutDiet.com. 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!
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 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?
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
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
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
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.
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.
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
Pulse Fast For Mass Phases
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:
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.
· 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.
Cabbage (green and red)