Inflammation for Muscle Growth

If you have been weight lifting for a year or more and read magazines and the internet for information, you probably have come across the topic of Inflammation. You have certain people in the industry promoting anti-inflammation for fat loss and muscle growth and other industry experts advocating inflammation for protein synthesis and fat loss as well. When I mention inflammation I am referring to inflammation derived from nutrients in food such as fatty acids. High dose fish oil has been touted as a major player in regulating inflammation from a nutritional stand point, and arachidonic acid has been hyped up as a pro inflammatory muscle builder by supplement companies. How can two polar opposite fatty acids elicit the same results for building muscle and decreasing body fat? The simple answer is: they don't. I have experimented first hand with high dose fish oil and olive oil and also high doses of arachidonic acid from red meat, egg yolks and various cheeses. I will share with you the effects that I got from both ends of the fatty acid spectrum when dieting for extreme fat loss.

Pro-Inflammatory                                               Anti-Inflammatory

After reading several articles from a popular trainer and author on a famous website that is revolved around testosterone and selling their own products, I took notice of his advice regarding extremely high dose fish oil. He was not just recommending 4-6 softgels a day, but up to 40 softgels a day of your standard 1000 mg product! After devising a plan of action about what products I was going to use and how I was going to orchestrate my diet, I would give this method a go. I planned on utilizing a low carbohydrate diet with carbohydrates only coming from green vegetables which bare minimal impact on blood sugar. I also chose liquid fish oil and olive oil for my only fat sources. The two oils were dosed at 4 tablespoons a day. Saturated fat from egg yolks and red meat were not present as I really wanted my omega 3 and omega 9 levels sky high.


4 tbs of carlson's fish oil
19,200 mgs EPA = 6,000 mgs DHA


4 tbs of olive oil
= 44 grams of monounsaturated fat


I was ready to dive right in and become joint pain free and absolutely shredded from oxidizing fat from increased uncoupling proteins. I was already in very respectable condition prior to starting this cutting phase. I had my abs displaying with a pretty thin skin fold measurement and of course arms were lean and vascular, I would say I was 9-11% maximum in body fat. My mass gaining diet prior to starting was still low carbs, but high in red meat from burgers, bacon, cheese, and peanut butter.

So the experiment began…

I was adamant about not ingesting nuts or nut butters as I really felt I would achieve optimal results from suffering with just oils and keeping trace carbs to a minimum. After the first week I began to notice some cosmetic changes. I felt like my muscle bellies were flat and deflating slightly, I also noticed my pronounced vascularity was less prevalent. My joints felt nice, but I really felt softer and smaller. I just assumed this was an awkward period from transitioning into a dieting phase from a mass gaining phase, and after 3-4 weeks, things will swing my way.

Week 3 arrived and a moment of reality hit me like a ton of bricks when a friend came into my work to talk to me. The very first thing he said when he saw me was "What happened to you? You look like crap?" "You looked bigger and leaner before you started your diet, what the hell is going on?" I immediately took offense and asked him what his problem was and he doesn't know what he's talking about, but after 5 minutes I knew he was absolutely right. I explained to him that I was experimenting with high dosages of essential fatty acids, namely omega-3 and omega-9 and that it is supposed to do all of these awesome things for fat-loss amongst other benefits. He quickly told me to ditch this protocol and do what I have always done because this obviously wasn't meshing well with my body type. Like I mentioned earlier, I already felt the signs of this diet going south from the first week and knew I had to switch gears and get myself back on track.

"What happened to you? You look like crap?"

I know that I am ectomorphic in nature and have always had a blazing metabolism. This made it very difficult building muscle and gaining weight. I knew from my past offseason that I respond extremely well to saturated fats. My new diet now consisted of lean red meat, whole eggs, whey isolate shakes with added egg yolks, light mozzarella cheese, and natural peanut butter. I would perform a carbohydrate refeed twice a week, on Thursday and Sunday for a 4 hour period.

Previous diet menu:           New diet menu:

-Olive oil                                             -Steak

-Fish oil                                              -Whole eggs (added yolks)

-Chicken breast                               -Cheese

-Whey isolate                                   -Peanut butter

After 1 week of switching from high dosages of fish oil and olive oil to an arachidonic acid rich diet, the changes to my physique were dramatic. My muscles began to swell and fill out, my vein protrusion was magnified, and my physique tightened up considerably. As the weeks flew by I got into better condition while maintaining muscular fullness even without the presence of carbohydrates. This solidified my thoughts regarding saturated fats being beneficial for ectomorphic hard gainers, and high fish oil being favorable for the huskier, endomorph body types.


Naturally lean ectomorphs
= High arachidonic based diet


Naturally husky endomorphs
= High fish oil based diet


From current literature it is widely accepted that ectomorphs have sufficient insulin sensitivity and higher metabolic rates. Endomorphs typically display insulin resistance issues and do very poorly with processing glucose, and also struggle with dropping body fat. Studies have demonstrated that saturated fat can increase insulin resistance by suppressing GLUT-4 production which reduces glucose transport significantly. However, for the ectomorph body type this shouldn't pose any threat. Saturated fatty acids have also been shown to increase testosterone production and increase prostaglandin formation from a class of substances called eicosanoids. Saturated fat found in red meat, animal organs, and egg yolks contain high amounts of arachidonic acid, which ultimately gets converted into the prostaglandin PGF2a. Once converted to PGF2a, it can begin doing it's magic.

Pgf2a has been shown to inhibit adipogenesis through mitigating the activation of mitogen-activated protein kinase. Arachidonic acid is also speculated to increase protein synthesis by the muscle being stretched from training and releasing prostaglandins PGF2a and PGE2. PGE2 is paramount in its role to induce satellite cell proliferation and fusion. This chain of events will increase the amount of nuclei in the cell which correlates to rapid muscle growth from mRNA production. These are just some of the attributes associated with consuming high amounts of inflammatory inducing fatty acids.

As you can clearly see from my personal experience and the facts listed, that for the hard gainer, following a pro inflammatory based diet is optimal for muscle growth and lean mass retention. For the individuals who have naturally higher body fat levels and struggle to shed fat, I would say having higher dosages of omega-3 is advisable. Not excessive amounts like the article I read from that website, but at least 8-12 softgels a day. I personally believe all body types should keep carbohydrate intake low to moderate, but especially endomorphs need to be very meticulous with their carbohydrate consumption if they value a favorable body composition.

Schematic summary of the biosynthetic pathway for eicosanoids derived from arachidonic acid.

Please understand that I experimented with such a diet while keeping my insulin levels extremely low, due to being on a ketogenic type of diet. If consuming copious amounts of carbohydrates I would definitely not implement excessive amounts of saturated fats due to health implications that could arise. In retrospect, I realized that this type of nutrition plan worked great for me, but I now firmly believe in nutritional balance. I advise people to consume both types of fats in equal ratios combined with low carbohydrate allotment.


1.)Juan J. Moreno*, T. Carbonell, T. Sánchez*, S. Miret and Maria T. MitjavilaOlive Oil Decreases both Oxidative Stress and the Production of Arachidonic Acid Metabolites by the Prostaglandin G/H Synthase Pathway in Rat Macrophages 3J. Nutr. August 1, 2001vol. 131 no. 8 2145-2149.

2.)Courtney E. Leik PhD, Scott W. Walsh, PhD. Linoleic Acid, but not Oleic Acid, Upregulates Production of Interleukin-8 by Human Vascular Smooth Muscle Cells via Arachidonic Acid Metabolites Under Conditions of Oxidative Stress.doi: 10.1016/j.jsgi.2005.09.004Reproductive Sciences December 2005 vol. 12 no. 8 593-598

3.)Andersson, A., A. Sjodin, A. Hedman, RM. Olsson, and B. Vessby. Fatty acid profile of skeletal muscle phospholipids in trained and untrained young men. Am J Physiol Endocrinol Metab. 279:E744-751, 2000.d profile

4.)Shephard, R. J. and P.N. Shek. Immune responses to inflammation and trauma: a physical training model. Canadian Journal of Physiology and Pharmacology 76: 469-472, 1998.

5.)Rajaram S, Connell KMSabaté J. Effect of almond-enriched high-monounsaturated fat diet on selected markers of inflammation: a randomised, controlled, crossover study. Br J Nutr. 2010 Mar;103(6):907-12. Epub 2009 Oct 29.

6.)Teruo Kawada,* Shun Kayahashi, Yoshifumi Hida,Ken-ji Koga, Yoshitaka Nadachi, and Tohru Fushik, Fish (Bonito) Oil Supplementation Enhances the Expression of Uncoupling Protein in Brown Adipose Tissue of Rat. J. Agric. Food Chem., 1998, 46 (4), pp 1225–1227

7.)DJ Maron, JM Fair and WL Haskell, Saturated fat intake and insulin resistance in men with coronary artery disease. The Stanford Coronary Risk Intervention Project Investigators and Staff. Circulation, Vol 84, 2020-2027, Copyright © 1991 by American Heart Association.

8.)Dorgan JFJudd JTLongcope CBrown CSchatzkin AClevidence BACampbell WSNair PPFranz CKahle LTaylor PR, Effects of dietary fat and fiber on plasma and urine androgens and estrogens in men: a controlled feeding study. Am J Clin Nutr. 1996 Dec;64(6):850-5.

9.)Zalin RJ The role of hormones and prostanoids in the in vitro proliferation and differentiation of human myoblasts. Exp Cell Res. 1987 Oct;172(2):265-81.

10.)Palmer RM. Prostaglandins and the control of muscle protein synthesis and degradation. Prostaglandins Leukot Essent FattyAcids. 1990 Feb; 39(2):95-104

The Power of Nicotine for Getting Lean

When you think of people who are addicted to smoking cigarettes, what type of person do you envision? I personally think of someone thin, drawn, and hyper-active.

When you hear about people trying to quit their smoking habits you typically hear about weight gain and increased hunger. This has to account for something right? I am sure most of you are thinking “smoking obviously suppresses appetite and that is why people stay leaner.” While that may be true – there is more to this fat shedding drug in regard to directly influencing lipolysis.  

You see, nicotine actually plays a vital role as a stimulant in the sympathetic nervous system. Nicotine increases catecholamine release (Epinephrine, Norepinephrine & Dopamine) in the adrenal glands. Remember in health class the “Fight or Flight” hormone? That is exactly what catecholamines are.

Speaking of catecholamines, dopamine is a great appetite suppressant as it aids in satiety due to increased dopaminergic activity in the brain. Also, when adrenaline is increased from elevated Epinephrine and Norepinephrine your basal metabolic rate increases as well as fatty acid oxidation via UCP-1 (uncoupling proteins) which then get activated in Brown Adipose Tissue (BAT) and also White Adipose Tissue (WAT).

Brown Adipose Tissue (BAT) is highly thermogenic and can be broken down readily opposed to White Adipose Tissue (WAT). Brown Adipose Tissue (BAT) is loaded with an abundance of blood-filled capillaries and variable size of lipid droplets.  The reasoning for BAT’s thermogenic properties are due to the expression of mitochondrial uncoupling proteins (UCP1) which initiates the cells mitochondria to uncouple fatty acids into the blood stream for use as an energy substrate opposed to ATP/Glucose. 

What about White Adipose Tissue (WAT)? This ugly adipose tissue is located directly beneath your skin and is called subcutaneous fat. WAT supplies cushion, support, and insulation as a defense mechanism for human survival. Too much of it can get ugly and not to mention – UNHEALTHY.

          Nicotine incinerates BOTH types of fat 

Scientists in Japan performed a study on mice that demonstrated fat-loss from nicotine usage in Brown Adipose Tissue (BAT) but also White Adipose Tissue (WAT). They treated obese mice with nicotine for 6 months and obese mice with a placebo saline solution for the same duration.  The mice receiving the nicotine consumed less food than those injected with saline, however, the mRNA and protein of UCP1 was detected in not only BAT but White Adipose Tissue as well. This indicates that nicotine can help mitigate the effects of obesity from various mechanisms.

Even more exciting, is the fact that when you add caffeine into the equation (100 mgs) + 1 mg of nicotine you can increase the thermogenic effect by 100%! Increasing the nicotine dose to 2 mgs did NOT increase the thermogenic effect more than 1 mg. It just increased unwanted side effects.  Caffeine stacked with nicotine speeds the rate of energy substrate usage in fatty acids and glucose metabolism. This is thought to have a “nutrient partitioning” effect and therefore help facilitate the storage of nutrients into muscle cells opposed to fat cells.

The "not so optimistic" part of the article  

As you know by now, nicotine is a stimulant and like most stimulants, an increase in blood pressure is accompanied with nicotine usage as well as vaso-constriction upon endothelial cells. This is caused by the catecholamine release which initiates epinephrine stimulation. This is not a desirable effect and should raise concern if thinking about incorporating nicotine into your weight loss regimen. Keep in mind that cigarettes have toxic tar in them and the smoke is polluted with carbon monoxide, which works in concert with nicotine to further narrow blood vessels for impaired  blood flow to the heart. Lung cancer is induced from excessive exposure to the cigarette smoke which is a carcinogen. Nicotine itself, is not cancerous however.       

         Benefits of Nicotine   

  • Increased focus and memory from presynaptic nerve terminals of dopamine, acetylcholine & glutamine secreting neurons.
  • Increased lipolysis from catecholamine release.
  • Anti-Depressant effects from dopamine stimulation.
  • Nutrient Partitioning Effect from increased blood flow to skeletal muscle.
  • Decreased Hunger.

          Negative Side Effects of Nicotine 

  • Addictive 
  • Raises Blood Pressure
  • Constricts Blood Vessels
  • Adrenal fatigue

So how would you put this information to use?

The cleanest way to get the benefits of nicotine without ingesting, inhaling or snorting tobacco would be to acquire nicotine chewing gum or a nicotine dermal patch. Remember that you only need 1 mg of nicotine combined with 100 mg of caffeine for enhanced fat loss. So, 1 mg of nicotine + 100 mg of caffeine 3 times per day spaced 4 hours apart would be most effective. The nicotine based gum comes typically in 2 mg and 4 mg dosages. So you can tear them in halfs or quarters to meet the 1 mg needed. The patch is tricky and I would not recommend it as it takes around 3 hours to finally "kick in" and will continuously supply your blood stream with nicotine whether you like it or not…

The patches come in extra strength,  (21 mg) medium strength,  (14 mg) and lower strength at (7 mg) — Which is the dosage you would need (7 mg). 

If you do try such an experiment in your quest for ultimate leanness – PLEASE take precautionary measures. The herb hawthorn berry in liquid extract form dosed at 900-1200 mg alleviates elevated blood pressure, dilates blood vessels, and assists in proper blood flow to the heart. A quality omega-3 fish oil supplement will also help aid in healthy blood pressure management and help regulate optimal blood flow to the heart. 



1.) Andersson K, Arner P.Systemic nicotine stimulates human adipose tissue lipolysis through local cholinergic and catecholaminergic receptors. Int J Obes Relat Metab Disord. 2001 Aug;25(8):1225-32.

2.) Keiko Arai,Kyongsong Kim, Katsumi Kaneko, Mitsue Iketani, Asuka Otagiri, Naoko Yamauchi, and Tamotsu Shibasaki.Nicotine infusion alters leptin and uncoupling protein 1 mRNA expression in adipose tissues of rats.Submitted 6 September 2000. accepted in final form 7 February 2001.

3.) Asuka Mano-Otagiri, Azusa Iwasaki-Sekino, Hisayuki Ohata, Keiko Arai, Tamotsu Shibasaki.Nicotine suppresses energy storage through activation of sympathetic outflow to brown adipose tissue via corticotropin-releasing factor type 1 receptor. Neuroscience Letters (2009) Volume: 455, Issue: 1, Pages: 26-29

4.) Jessen AB, Toubro S, Astrup A.Effect of chewing gum containing nicotine and caffeine on energy expenditure and substrate utilization in men. Am J Clin Nutr. 2003 Jun;77(6):1442-7.

5.) T Yoshida, N Sakane, T Umekawa, A Kogure, M Kondo, K Kumamoto, T Kawada, I Nagase, M Saito.  Nicotine induces uncoupling protein 1 in white adipose tissue of obese mice. 06/1999; 23(6):570-5.
6.) William T. ChanceCorresponding Author Contact Information, a, Teri Foley-Nelsona, Jeffrey L. Nelsona and Josef E. Fischera. Neurotransmitter alterations associated with feeding and satiety. Volume 416, Issue 2, 28 July 1987, Pages 228-234 

Lipoprotein Lipase Important for Fat Burning

Lipoprotein lipase important for fat burningJanuary 7th, 2010 – Lipoprotein lipase (LPL) is an enzyme that breaks apart fat (triglycerides) into their fatty acid components for transport and use inside cells.

An increase in lipoprotein lipase activity means an increase in the flow of fatty acids into the cell.  An increase in LPL activity in muscle cells means they will use more fat and less sugar for energy, which is a good thing if you are trying to stay lean.  An increase in LPL activity in fat cells, however, will mean increased fat stores.  There are many factors involved in the regulation of LPL activity, but two big contributors are the hormones insulin and testosterone.

Insulin increases LPL activity in fat cells, while decreasing LPL activity in muscle cells.  (1) Anything that drives up insulin (mainly dietary carbohydrates) will increase the flow of fatty acids into fat cells for storage and cause muscle cells to burn sugar instead of fat.

Testosterone also has a regulatory effect on LPL activity in muscle. Lipoprotein lipase activity in the fat cells of the abdominal region is greater in men than in women, and reduced testosterone levels only increases activity.  Keeping testosterone levels high, however, works to reduce LPL activity in the male abdominal fat cells thus discouraging fat storage in this area. (2)

References –

1. Lipoprotein lipase regulation by insulin and glucocorticoid in subcutaneous and omental adipose tissues of obese women and men.

Fried SK, Russell CD, Grauso NL, Brolin RE.

J Clin Invest. 1993 Nov;92(5):2191-8

2. Good Calories Bad Calories

Gary Taubes

Alfred A Knopf 2007 Pages 397-399

Lectins in Peanuts Clog Arteries

Lectins in peanuts clog arteriesNovember 25th, 2009 –A peanut butter and jelly sandwich on whole grain bread looks pretty wholesome and harmless, doesnít it? Well, looks can be deceiving. This delicious meal is packed with a deadly lectin that clogs your arteries.

The trouble seems to stem from a lectin specific to peanuts called Peanut Agglutinin(PNA). Lectins are sugar-binding proteins found all throughout nature, and are thought to play an important role in plant defense against being eaten. (1) PNA is particularly resistant to breakdown in the gut, and has been shown to penetrate the intestinal walls mostly intact and bind to the smooth muscle cells in the arteries, leading to atherosclerosis (build-up of plaque within the arteries) and fibromuscular lesions. (2) Aside from being a know allergen, PNA has also been shown to stimulate cellular proliferation of colon cancer cells (3).

Even if you donít have any peanut allergies, eating peanuts may still increase your heart disease and colon cancer risk. Peanuts have side-effects, so you are probably safer choosing almond butter for that next ìnut butterî sandwich.

References –

1. Agrarian Diet and Diseases of Affluence – Do Evolutionary Novel Dietary Lectins Cause Leptin Resistance?
Tommy J?nsson, et al.
BMC Endocrine Disorders 2005, 5:10doi:10.1186/1472-6823-5-10

2. Atherogenic Potential of Peanut Oil-Based Monounsaturated Fatty Acids Diets
Loren Cordain, Ph.D.
Lipids 1998 Vol. 33 no. 2 Page 229

3. Peanut lectin stimulates proliferation of colon cancer cells by interaction with glycosylated CD44v6 isoforms and consequential activation of c-Met and MAPK
Singh R et al.
Glycobiology.2006 Jul;16(7):594-601.

%d bloggers like this: