Just say the name a few times and you will get the hint!!
* Appetite suppression
* Increase energy and focus
* Mood enhancement
* Fat oxidation
* Cortisol and insulin regulation
* Increase physical endurance
The White Willow Tree (salix alba), also known as European Willow, is native to central and southern Europe. For centuries the bark from this
willow tree, and others such as the Purple Willow Tree (salix purpurea), have been used in traditional medicine for its pain relieving and antiinflammatory properties. The active ingredient in willow bark is salicin and when consumed our bodies convert this chemical into salicylic acid,
similar in structure to modern day aspirin (acetlyl salicylic acid). Often you'll hear willow bark referred to as “herbal aspirin” as it works in much
the same way. The main difference between the two being willow bark will take longer than aspirin to act but its effects may last longer,
however willow bark's pain relieving properties will not be as pronounced as aspirin's. There is little evidence that willow bark by itself
promotes or enhances weight loss. However when willow bark is combined with thermogenic ingredients such as Caffeine Anhydrous, 1,3-
Dimethylamlamine or Yohimbine HCL, it's thought to extend or enhance their fat burning properties.
A yohimbine-isomer that works with far more potent MAOI-inhibiting properties (normally, yohimbine isn't very strong in this regard). Because
of this, it basically works as an amphetemine-potentiator, because it prevents the neuro-breakdown of the brain's 'big three'-- serotonin,
noradrenaline, and dopamine. It also has similar alpha-2 antagonistic properties to yohimbine HCl, but is also less vasoconstrictive in areas,
making it less likely to induce large increases in BP.
Alpha-yohimbine (Alpha-Y) is an analogue of yohimbine, but its potency at the subreceptors of alpha2 differ quite a bit--most notably at the
alpha2b and alpha2c adrenergic subreceptors. It is 3 times more potent at alpha2b and 4 times more potent at alpha2c. It is equipotent at
alpha2a. The differing ratios of activity is where it allows us to do good stuff with it that we could not do with yohimbine.
Alpha2a mediates most the classic effects of alpha2 receptor agonists and antagonists. There is plenty of info on this in regard to the
equipotent yohimbine, so I will not get into it, except to say its superior potency at the other receptors lets us use less to hit them, so we can
minimize the negatives here – namely, an increase in heart rate, blood pressure, anxiety, and norepinephrine (NE) hyperactivity, centrally.
The alpha2c receptor plays a minor role in the negative feedback signal on NE, but it plays a major role in certain brain areas where sympathetic
innervation is low, and the dopamine system is prominent, which just happen to be the areas that are critical for reward, reinforcement, and
metabolic control, such as the VTA and striatum. In these areas, dopamine--not NE--is the primary agonist at alpha 2 receptors, and alpha2c
makes up the majority of these receptors. So, it will block dopamine’s negative feedback signal, thus increasing dopaminergic tone.
If that were not handy enough, the only other place the alpha2c receptors are highly expressed is in the adrenal medulla, where it modulates
negative feedback on epinephrine (E), much like alpha2a does on NE. In other word, alpha-y allows for a much greater increase in E levels, with
its superior effect on thermogenesis, energy expenditure, and nutrient partitioning.
The alpha2b receptor is prominent in development (it is the only adrenergic deletion that impacts survival), but in adults, it only affects blood
pressure. Namely, it increases the hell out of it, especially in regard to salt loading. In the obese, and with overfeeding, receptor levels are
upregulated. Not coincidentally, it also increases Arginine vasopressin activity. And, if you have read my Ab-Solved write-up, and the leptin
series on our site, you might note how strongly tied in obesity, blood pressure, and the renin-angiotensin/cortisol systems are. So, not only are
we minimizing the increase in the alpha2b agonist NE, we are blocking the receptor more strongly than with yohimbine.
Caffeine anhydrous is simply caffeine in dehydrated form, without the water. If one takes a pill containing caffeine anhydrous,
one might as well drink a cup of coffee for the same effect, although the concentration of caffeine may differ between the two.
Rather than paying much attention to words portraying caffeine anhydrous as some new miracle drug, simply think "caffeine".
That's not to say there's anything wrong with caffeine anhydrous pills or supplements.. They are known to have value in a
weight reduction program as, like the caffeine in coffee, they speed up the metabolism causing calories to be burned at a more
rapid rate. The pills can also be a powerful stimulant.
Recent evidence suggests that 3,5-diiodo-L-thyronine (T2), a naturally occurring iodothyronine, stimulates metabolic rate via mechanisms
involving the mitochondrial apparatus. In addition, T2 can induce metabolic inefficiency, possibly by stimulating energy loss via mechanisms
involving mitochondrial proton leakage/redox slippage. Such inefficiency in energy transduction should result in reduced energy storage. In
view of these metabolic effects of T2 and the very low affinity of T2 for nuclear T3 receptors, we thought it conceivable that in rats fed a high-fat
diet (HFD), long-term treatment with T2 might result in a reduced adiposity and less body weight gain without inducing a clinical syndrome
related to the thyrotoxic state. 3,5-diiodo-l-thyronine (T2) has been shown to exert marked effects on energy metabolism by acting mainly at
the mitochondrial level. Here we investigated the capacity of T2 to affect both skeletal muscle mitochondrial substrate oxidation and
thermogenesis within 1 h after its injection into hypothyroid rats. Administration of T2 induced an increase in mitochondrial oxidation when
palmitoyl-CoA (+104%), palmitoylcarnitine (+80%), or succinate (+30%) was used as substrate, but it had no effect when pyruvate was used. T2
was able to 1) activate the AMPK-ACC-malonyl-CoA metabolic signaling pathway known to direct lipid partitioning toward oxidation and 2)
increase the importing of fatty acids into the mitochondrion. These results suggest that T2 stimulates mitochondrial fatty acid oxidation by
activating several metabolic pathways, such as the fatty acid import/β-oxidation cycle/FADH2-linked respiratory pathways, where fatty acids are
imported. T2 also enhanced skeletal muscle mitochondrial thermogenesis by activating pathways involved in the dissipation of the protonmotive force not associated with ATP synthesis (“proton leak”), the effect being dependent on the presence of free fatty acids inside
mitochondria. We conclude that skeletal muscle is a target for T2, and we propose that, by activating processes able to enhance mitochondrial
fatty acid oxidation and thermogenesis, T2 could play a role in protecting skeletal muscle against excessive intramyocellular lipid storage,
possibly allowing it to avoid functional disorders. adenosine 5′-monophosphate, thyroid hormone, mitochondria among the endocrine factors
able to regulate substrate metabolism and thermogenesis, thyroid hormones (THs) play important roles. 3,5,3′-Triiodothyronine (T3) exerts a
plethora of effects, including upregulation of peripheral and hepatic glucose uptake, cholesterol reduction, loss of body weight and adiposity, cardiac acceleration, and increases in metabolic rate. In adults, T3 regulates energy metabolism by increasing respiration and energy
expenditure and by lowering metabolic efficiency .Because of this, T3 was tested in the past as an antiobesity and hypolipidemic agent.
O-methoxy phenyletylamine, Beta phenylethylamine, 4-hyroxyphenylethylamine, N-dimethylhydroxyphenletylamine(PEA)
Well, besides being terribly difficult to pronounce Phenylethylamine, or PEA is an ingredient that can be found in a few weight loss products.
Phenylethylamine can be found in chocolate (as well as many illegal drugs like LSD). Phenylethylamine, or PEA, is a neuromodulator, which is
responsible for the transmission of norepinephrine and dopamine. PEA is also known as the “love drug”, and is the primary reason why
chocolate is considered an aphrodisiac. This is a much more efficient way to experience the mood enhancing properties of chocolate without
the fat and extra calories. Phenylethylamine is a stimulant in which some also believe that it has the ability to suppress the appetite along with
being a strong mood enhancer as well. Besides enhancing mood, phenylethylamine also elevates mental alertness because it releases
acetylcholine, which supports memory and cognitive skills, such as concentration.
As a metabolic intermediate for the biosynthesis of Serotonin and Melatonin from Tryptophan, 5-Hydroxytryptophan (5-HTP), a naturally
occurring amino acid, is widely used as an OTC dietary supplement for the effective treatment of depression, chronic headaches, pre-menstrual
syndrome, over eating and sleeplessness. Many people who experience depression seek to elevate their Tryptophan/Serotonin levels by
consuming a diet low in protein and high in carbohydrates and processed foods; the higher the protein intake, in fact, the harder it is for them
to establish normal Tryptophan levels in the brain. With the addition of 5-HTP, Serotonin levels can be boosted without the extreme practice of
overeating. 5-HTP will also diminish one’s appetite to prevent them from gorging on the wrong foods. Therefore, weight loss and improved
mental function are the major benefits of supplementing with 5-HTP.
Tea is the most-consumed hot beverage all over the world. Tea is available in different forms like black tea, green tea and white tea, depending
on its ingredients. Black tea is prepared from a plant called Camellia sinesis. The old leaves and the stem of the plant are used in the
preparation of black tea. Black Tea improves the mental alertness of patients suffering from severe stress and depression and prevents
aggravation of the condition. It improves the memory and learning skills of the person. Lack of these skills can lead to depression and stress in
patients. Consuming black tea improves these skills and reduce stress. It enhances our information processing skills. It helps in rapid analysis by
our brain and thus helps in avoiding stressful conditions. It helps in reducing repeated attacks of headache in patients suffering from stress and
depression. Drinking black tea increases the basal metabolic rate of the body, which helps in increasing the energy consumption of our body.
The food that is eaten is utilized by the body at a faster rate. Thus, black tea can help in reducing the calorie intake of our body. Also, black tea
can burn fat at a higher rate and so helps obese people to get rid of excess fat in the body. The fat is mobilized from the fat deposits and
converted into energy for its utilization at an increased rate. This helps patients who want to lose weight. Black tea contains several antioxidants that help in detoxifying our body to get rid of unwanted toxins. So, black tea assists in weight loss in a healthy manner unlike other
methods used for weight loss. Hence, it can be concluded that there are several benefits of black tea for stress, diabetes and weight loss in
patients suffering from them. It should be noted that black tea may lose some of its beneficial properties if mixed with milk. Regular
consumption of black tea can help patients to relieve their anxiety and live a stress-free life. It can benefit a lot of people as it helps in
prevention of diabetes, which is the commonest metabolic disease all over the world. It helps obese patients in their weight loss programs as it
helps in reducing their weight in a harmless and healthy manner. Consuming black tea will help in weight loss when coupled with dietary
restrictions and regular exercises.