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How many men find themselves relatively lean, but still having trouble getting that last little pinch (or grab!) off of their lower abs and love handles? And I know we've all known at least four or five women who swear that the only place they cannot lose fat is their butt and thighs. What gives?
Simply put some areas in the body have more receptors that block fat breakdown than receptors that increase fat breakdown. In men these areas are the lower abs and love handles; in women they are the thighs and butt.
In order to lose this last bit of stubborn fat you will have to diet and train more intensely. Sometimes that doesn't work or is just straight up not possible. This is where specific dietary supplements that target fat loss come into play. In this article we will briefly look at some of the physiological factors controlling fat loss and then go over beneficial fat loss supplement.
Norepinephrineand Adrenergic Receptors
Body fat storage is controlled by many different factors ranging from diet to hormones to receptor density. Of importance to this article is receptor density. Without diving to deep into the nerdy science stuff, a receptor can be looked at like a lock that a key (i.e. a hormone) fits into.
The term "adrenaline" is commonly used to refer to the body's excitatory catecholamines, Epinephrine (E) and Norepinephrine (NE), which are regulators of lipolysis (fat breakdown). NE and E acts on receptors called adrenergic receptors of which there are alpha (1 & 2) and beta (1, 2, & 3) subtypes.
Activation of the alpha1 and beta-receptors is lipolytic (causes fat breakdown) while activation of the alpha2 receptor is anti-lipolytic (blunts fat breakdown). Stubborn fat areas have a high density of alpha2 receptors, making it harder for fat breakdown to occur in that area.
In order to burn stubborn fat we must override the inhibitory effect of the alpha2 receptors (which will be discussed later). Now that we know the cause of stubborn fat areas we need to learn how to burn the fat!
Stored Triglycerides-Body Fat We Want To Lose
While all cells contain some fat, it is mainly stored in muscle (intramuscular triglycerides) and in adipose tissue (body fat). Adipose tissue is the body's main fat storage site and the fat we all want to lose.
Adipose tissue is divided into individual cells called adipocytes. These adipocytes hold stored triglyceride (1 glycerol molecule bonded to 3 fatty acids) droplets, which serve as a source of energy for the body. These droplets make up 95% of adipocytes' volume. In order for this storage of potential energy (60,000-100,000 kcal) to be used and to LOSE BODY FAT (everyone's goal), it must be mobilized through lipolysis (the breakdown of triglycerides).
Lipolysis involves splitting the triglycerides into a glycerol molecule and 3 separate fatty acids (FFA). Once the fatty acids diffuse (exit) from the adipocytes, they bind to plasma albumin (a protein in the blood) in order to be transported to active tissues where they can be burned. In order to lose body fat, the fatty acids must be burned!
Transport Of FFA To Be Burned!
Blood flow is of prime importance to the transportation of FFA away from adipocytes and through the circulation to active tissues where they can be burned. This is especially important during exercise where energy requirements are heightened.
Low blood flow could cause the accumulation of FFA within adipose tissue resulting in less available FFA to be oxidized and a greater chance of FFA to be turned back into triglycerides. What is the best way to increase blood flow? Exercise! In addition to this certain supplements can also increase blood flow (more on this later). Increasing blood flow throughout the body will assist in losing weight by transporting FFA to where they can be burned.
Click Image To Enlarge. Derek Charlebois.
FFA Oxidation-Burning Body Fat
When the FFAs reach muscle tissue, they are transported into a muscle cell. Once in the muscle cell, the FFAs can re-esterfy (rebind) with glycerol to form triglycerides to be stored in the muscle or bind with intramuscular proteins to be used for energy production in the mitochondria. In the mitochondria, the fatty acids undergo beta-oxidation, meaning they are burned for energy.
We want the FFAs to be burned in the mitochondria. Increasing energy demands through exercise is the best way to accomplish but there are supplements that can help give you an extra boost.
Summary Thus Far
- Stubborn fat areas are caused by a high density of Alpah2 receptors
- Lipolysis must be increased in order for FFAs to be burned
- Blood flow to adipose tissue and transportation of FFAs away from adipose tissue is vital to fat loss
- FFAs must be BURNED to body fat loss to occur
- Exercise is the best way to increase blood flow to adipose tissue, transportation of FFAs, and oxidation of FFAs
Supplements
Knowing these facts allows us to choose supplements that will assist in burning through stubborn fat. Let's look at some supplements that can help burn stubborn fat.
Yohimbine HCL
Yohimbine is an alpha2 receptor antagonist (Kucio, 1991), which means it inhibits the action of the alpha2 receptor. By blocking the alpha2 receptor with Yohimbine, the negative feedback caused by NE binding to the alpha receptors is reduced and fatty acid liberation is increased.
Yohimbine has been shown to increase fat loss (Kucio, 1991) by increasing the amount of fat mobilization and oxidation (Berlan, 1991) and blood flow to adipose tissue due to alpha2 antagonism (Galitzky, 1993). So Yohimbine addresses two of the stubborn fat issues we are trying to correct: alpha2 receptor action and blood flow.
Caffeine
Caffeine, a plant alkaloid belonging to the drug class methylxanthines and is found in natural sources such as coffee beans, tea leaves, cocoa beans, and other plants, is the world's most widely used stimulant. Caffeine is a Central Nervous System (CNS) stimulant shown to delay fatigue and improve cognitive performance.
Caffeine acts as an adenosine receptor antagonist. Adenosine decreases the release of stimulatory/excitatory neurotransmitters (i.e. norepinephrine [NE]). Therefore, blocking the adenosine receptor allows a greater excitation to occur by increasing NE's ability to activate the adrenergic receptors.
Caffeine inhibits phosphodiesterase (PDE), causing a build-up of cAMP levels and greater effect of NE on fatty acid lipolysis. PDE blunts lipolysis; therefore inhibiting PDE allows lipolysis to proceed at an accelerated rate. The end result is there are more fatty acids available for oxidation after consumption of caffeine. Caffeine addresses the need to increase fat lipolysis so that FFAs can be burned and body fat can be lost.
ALCAR
The amino acid L-Carnitine plays a vital role in energy metabolism, specifically the transport of fatty acids into mitochondria where they can be burned. ALCAR is the acetylated form of carnitine and is the most popular form of supplemental carnitine.
ALCAR is a potent antioxidant shown to have anti-aging, cardio-protective, cognitive enhancing, and adaptogen properties. ALCAR increases exercise performance by increasing fat oxidation (Hongu, 2003). ALCAR is believed to increase the transportation of FFAs into the mitochondria where they can be burned..
Green Tea Extract
The active in green tea is EGCG. EGCG has thermogenic effects and has been shown to assist in weight loss by decreasing dietary fat absorption, appetite suppression, and catechol-O-methyl-transferase (COMT) inhibition. COMT is involved in the breakdown of catecholamines (i.e. NE).
By inhibiting COMT, NE breakdown is slowed and it is able to activate the adrenergic receptors to a greater degree and enhance lipolysis. Green tea extract increases lipolysis, making more FFAs available to be burned.
Sesamin
Sesamin is a lignan isolated from sesame seeds. A lignan is a molecule that combines with another entity acting as an "activator." In the case of sesamin, it binds to and activates a receptor called Peroxisome Proliferator-Activator Receptor Alpha (PPARalpha). Sesamin has been shown to be a potent PPARalpha activator (Ide, 2003).
The PPAR receptor family is divided into three subgroups: alpha, beta/delta, and gamma. PPARalpha is highly expressed in muscle, the liver, kidneys, and heart and is involved in the regulation of fat metabolism. Activation of PPARalpha increases gene expression of the fatty acid oxidation enzymes and decreases gene expression of lipogenic enzymes. So Sesamin works in two ways to make you lean (and keep you lean): increasing fat oxidation and decreasing fat storage.
Supplement Summary
- Yohimbine blocks Alpha2 activation allowing for greater fat breakdown to occur and also increase blood flow to adipose tissue, making it perfect for targeting stubborn fat.
- Caffeine increase lipolysis by inhibiting the Adenosine receptor and PDE and also increases energy and delays fatigue.
- ALCAR increases the transportation of FFAs into the mitochondria and enhances fat oxidation.
- Green Tea Extract inhibits COMT thereby increasing lipolysis.
- Sesamin increases the genes involved in fat oxidation, increasing one's capacity to burn fat and also decreases fat storage.
The combination of Yohimbine+Caffeine+ALCAR+Green Tea Extract+Sesamin would make for the PERFECT Stubborn Fat Stack.
Click To Enlarge. Derek Charlebois.
References:
- Berlan M, Galitzky J, Riviere D, Foureau M, Tran MA, Flores R, Louvet JP, Houin G, Lafontan M. Plasma catecholamine levels and lipid mobilization induced by yohimbine in obese and non-obese women. Int J Obes. 1991 May;15(5):305-15
- Galitzky J, Lafontan M, Nordenstrom J, Arner P. Role of vascular alpha-2 adrenoceptors in regulating lipid mobilization from human adipose tissue. J Clin Invest. 1993 May;91(5):1997-2003
- Hongu N, Sachan DS. Carnitine and choline supplementation with exercise alter carnitine profiles, biochemical markers of fat metabolism and serum leptin concentration in healthy women. J Nutr 2003 Jan;133(1):84-9
- Ide T., et al. 2003. Sesamin, a Sesame Lignan, as a Potent Lipid-Lowering Food Component. JARQ 37 (3), 151 - 158.
- Kucio C, Jonderko K, Piskorska D. Does yohimbine act as a slimming drug? Isr J Med Sci. 1991 Oct;27(10):550-6
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