Topical LipoMorph — More effective, more targeted
LipoMorph has been reformulated for targeted fat reduction at the site(s) of application, while avoiding the negative side effects associated with systematic distribution.
LipoMorph is the first “fat burner” supplement to specifically target all known modifiable mechanisms of white fat browning, and both brown and beige fat activation.
Ordinary white fat stores energy in the form of fat droplets, one droplet per adipocyte, which can be broken down by lipolysis into free fatty acids which are circulated into the bloodstream and transported to the fuel-requiring tissue where they undergo beta-oxidation to acetyl-CoA which can be used to generate energy through the Krebs cycle. The energy stored in white fat, when liberated, is primarily burned to produce ATP to power cells.
Unfortunately, modern Western diet and lifestyle habits (consisting of excessive caloric intake typically coupled with insufficient physical activity) can cause an excessive accumulation of both subcutaneous and visceral white adipose tissue (WAT) that can have numerous adverse effects on health and health markers.
Brown fat is a thermogenic tissue that turns energy (stored as triglycerides) into heat. It’s found in abundance in hibernating mammals. When the temperature drops, animals like bears “go to sleep for the winter”. They’re able to survive by burning reserves of energy which have been stored as white and brown fat. The heat produced by the brown fat, which is activated by the cold, maintains the essential core body temperature of the animal through the winter months.
It’s also found in high quantities in babies, but is present in much smaller amounts in adult humans.
Unlike adults, babies are unable to regulate their own temperature by, say, putting on a coat or moving to a warmer room, so their ability to regulate their own temperature is more vital to their survival. Accordingly, they have greater amounts of brown fat which is widely distributed viscerally and subcutaneously, decreasing as age increases until as adults brown fat is largely limited to small deposits in the lower neck and supraclavicular region. These deposits are suspected to be useful in cold weather for warming blood as it flows to the brain. Brown fat appears brown in color because of the high density of mitochondria and excellent blood supply. Certain natural conditions, like endurance exercise and cold temperatures, can encourage the human body to produce and/or activate brown fat.
Thermogenesis in brown fat is mediated by thermogenin, also known as uncoupling protein 1 (UCP1). UCP1 is specific to the mitochondria of brown fat, and functions as a proton transporter, uncoupling oxidative phosphorylation from ATP synthesis and allowing the resulting energy to dissipate in the form of heat. The thermogenic effect of UCP1 is known as “non-shivering thermogenesis”.
In addition to classical brown fat, which originates from the same progenitor cells as muscle tissue, brown-like fat expressing the same thermogenic genes as brown fat can be made from regular mature white fat cells and their precursors. This brown-from-white fat is variously termed “brite” or “beige” fat, and the process of its creation known as “browning” of white fat. Whereas excessive white adipose tissue (WAT) impairs health, the recruitment and activation of brown and beige adipose tissue is currently being investigated as being potentially beneficial in the fight against obesity and metabolic disorders.
Regulators of brown and beige fat
Natural regulators of brown and beige fat include external conditions like cold temperatures, and exercise, as well as internal mechanisms like thyroid hormones, beta-adrenergic hormones, retinoids, PPARγ and PPARα agonists, and the liver X receptor.
What is it?
N-Coumaroyldopamine is a naturally-occurring phenylpropenoic acid amide found in plants such as cocoa.
• N-Coumaroyldopamine is a selective agonist of the mammalian beta-2 adrenergic receptor (β2 adrenoreceptor).
• Beta-2-adrenoceptor agonism is one of the primary regulators of brown fat activation and beige fat recruitment, via PGC1a, downstream.
What is it?
(−)-Menthol is a naturally-occurring terpene found in wild mint and peppermint.
• Menthol is an agonist of the TRPM8 receptor, also known as the cold and menthol receptor.
• TRPM8 activation triggers thermogenesis in brown fat by mimicking long-term cold exposure.
• Menthol is also an agonist of transient receptor potential A1 (TRPA1) in humans, another thermosensitive (cold-sensing) receptor that has been linked to brown fat activation in animal models.
What is it?
One of the forms of vitamin A is retinol. This animal-derived retinoid is essential for healthy skin, bone, and teeth. The main active metabolite of vitamin A is retinoic acid.
• Retinoic acid binds to and activates the retinoic acid receptor (RAR).
• The vitamin A metabolite 9-cis-retinoic acid is an endogenous ligand of the retinoid X receptor (RXR)
• Retinoic acid activates transcription of uncoupling protein-1 (UCP-1) both in vitro and in vivo.
• Retinoic acid is necessary for induction of human UCP1 by beta-adrenergic agonists.
• Retinal (retinaldehyde), another retinol metabolite, induces browning of white fat through activation of the retinoic acid receptor (RAR).
What is it?
Stearoyl vanillylamide is a naturally-occurring capsaicin analogue found in red pepper species. Capsaicin is responsible for the hot/burning feeling caused by chili peppers. Unlike capsaicin, stearoyl vanillylamide is nonpungent, meaning it does not impart the “spicy” or irritative effects of capsaicin.
• Stearoyl vanillylamide, capsaicin and similar compounds activate the transient receptor potential cation channel V1 (TRPV1).
• TRPV1 activation stimulates the release of catecholamines such as adrenaline and noradrenaline from the adrenal medulla. Noradrenaline is a major regulator of brown fat activation, through β3 adrenoreceptor activation.
• Nonpungent capsaicin analogs have been demonstrated to activate brown adipose tissue and increase energy expenditure in a human clinical trial.
• Chronic TRPV1 activation by dietary TRPV1 agonists can increase phosphorylated levels of protein kinase A (PKA) and endothelial NO synthase (eNOS), causing peripheral vasodilation and a decrease in blood pressure in hypertensive rats.
• The oral administration of TRPV1 agonists prevents adipogenesis and obesity in mice fed a high-fat diet.
• Stearoyl vanillylamide increased lipolysis and oxidation of free fatty acids in rats, resulting in increased capacity for exercise.
• Some non-pungent capsinoids have also been found to activate TRPA1, another receptor that may be involved in cold detection.
What is it?
Yohimbine is a naturally-occurring alkaloid derived from the bark of the tree Pausinystalia johimbe.
• Yohimbine is a selective antagonist of the mammalian alpha-2 adrenergic receptor (α2 adrenoreceptor).
• Activation of the alpha-2-adrenoceptor inhibits lipolysis and cyclic AMP accumulation, thus sabotaging adipocyte browning