Dear Enhancetech Customers
We wish you a joyful Christmas season and a happy new year!
I hope the holiday spirit stays with you throughout the year.
Love’s alchemy may do wonders for our moods, so let’s let it shine on our faces and hearts.
Enhancetech team
Dear valued regular and new customers!
We have happy to say that we have massive discounts. Up to 35% discount for all our provided SARMs and Nootropics. Black Friday Sale lasts november 24-26 because we consider with different time zones, and we want all our customers to take part in the discounts. No matter what part of the world they live in. Go to our store and take advantage of the good opportunity to purchase SARMs.
Cardarine, Ostarine and Ibutamoren are very different performance-enhancing research chemicals SARMs. All three have been moderately well researched.
Cardarine increases endurance and lipid metabolism. I´ts microdose elevates good cholesterol.
Ostarine mimics the anabolic effects of testosterone more selectively than anabolic steroids. It´s relatively non-toxic; alas, users of high doses have been hospitalized due to adverse effects similar to anabolic steroids (liver toxicity).
Ibutamoren is a synthetic analogue of hunger hormone. That alters the intensity rather than pattern of growth hormone secretion.
Larger doses have probably higher risk of adverse effects. Recently, it was even suggested that cardarine is dangerous when combined with a SARM (ostarine). While it may tempting to think that cardarine would be a good means to reduce the side effects of SARMs or ibutamoren, it may be a bad idea. Recently, it was suggested that combination of cardarine and ostarine is toxic. At least after prolonged use of the combination. The following table shows both desirable and undesirable effects of these three major performance-enhancing chemicals.
https://pubmed.ncbi.nlm.nih.gov/19852734/
https://pubmed.ncbi.nlm.nih.gov/31642815/
https://pubmed.ncbi.nlm.nih.gov/9467542/
https://pubmed.ncbi.nlm.nih.gov/18981485/
https://pubmed.ncbi.nlm.nih.gov/10372705/
https://pubmed.ncbi.nlm.nih.gov/9329386/
https://pubmed.ncbi.nlm.nih.gov/22814748/
https://pubmed.ncbi.nlm.nih.gov/14525954/
https://pubmed.ncbi.nlm.nih.gov/25854303/
https://pubmed.ncbi.nlm.nih.gov/17110604/
https://pubmed.ncbi.nlm.nih.gov/34678947/
https://pubmed.ncbi.nlm.nih.gov/20602678/
https://pubmed.ncbi.nlm.nih.gov/32876707/
https://pubmed.ncbi.nlm.nih.gov/29785666/
https://pubmed.ncbi.nlm.nih.gov/22031847/
https://pubmed.ncbi.nlm.nih.gov/24708238/
Phosphodiesterase 5 (PDE-5) inhibitors were originally investigated for hypertension because of their ability to relax blood vessels. To researchers’ surprise, inhibiting PDE-5 was even better for improving male erection. That’s why PDE-5 inhibitors such as sildenafil or tadalafil are most commonly marketed for improving erectile function. Relaxing blood vessels may be beneficial for purposes of exercise. PDE-5 inhibitors have potential to increase endurance performance because it counteracts contraction of blood vessels in lungs [1].
Clinical studies have shown that sildenafil and tadalafil can improve exercise capacity in certain patient populations. A proof-of-concept study demonstrated somewhat increased aerobic exercise capacity in young adult patients with cystic fibrosis, a disease that reduces lung function [2]. 25 mg of sildenafil increased the VOmax approximately 5% after four weeks of use while a single 50 mg dose failed to increase VOmax significantly despite some tendency to do so. There is some data that tadalafil increases exercise capacity of patients with pulmonary hypertension . It must be noted that the study subjects were those who could not walk 4.5 km/h for 10 minutes [3] and about third of the patients suffered from headache as an side effect.
In diabetic but not in healthy women, tadalafil has been shown to increase glucose utilization in the muscle [5]. In cyclists, sildenafil did not improve the results in the context of 16.1 km exercise [1]. On the negatice side, tadalafil is associated with yet unexplained higher incidence of back pain in clinical studies. About 8.3% to 9.4% of men taking tadalafil suffered from back pain while only 3.4% of men in placebo group suffered from back pain — the risk is greater than two-fold [6]. There was no difference in blood parameters. Hence, the increased incidence of back pain lacks explanation. One might ask if the back pain is associated with increased strenuous sexual performance. Anabolic steroid users seem to use PDE-5 inhibitors mainly for sexual enhancement also [7]. In mice, PDE-5 inhibitors can increase the production of testosterone [8].
In men – possible but unlikely. The scientific consensus based on several human studies is that PDE-5 inhibitors do not increase testosterone production. PDE-5 inhibitors are beneficial for semen but, again, in infertile rather than healthy men [9]. It seems unlikely that PDE-5 inhibitors augment testosterone. It is the other way around, instead [10]. PDE-5 inhibitors are sexual performance enhancers that just happen to be performance enhancers in serious lung disease patients.
Don´t hesitate to ask it.
[1] https://pubmed.ncbi.nlm.nih.gov/30653578/
[2] https://pubmed.ncbi.nlm.nih.gov/31803404/
[3] https://pubmed.ncbi.nlm.nih.gov/19470885/
[4] https://pubmed.ncbi.nlm.nih.gov/4377045/
[5] https://pubmed.ncbi.nlm.nih.gov/20535445/
[6] https://pubmed.ncbi.nlm.nih.gov/16034469/
[7] https://pubmed.ncbi.nlm.nih.gov/31303195/
[8] https://pubmed.ncbi.nlm.nih.gov/19659904/
[9] https://pubmed.ncbi.nlm.nih.gov/28259808/
[10] https://pubmed.ncbi.nlm.nih.gov/24251448/
Hi Enhancetech
Here’s a picture of me taken 2 months between this summer. In this period I used cardarine and ostarine. I combination with 2/4 protein, 1/4 carbs and 1/4 fats I felt the shredding process even after a few days. Luckily, as you can see, I had noticable gains in muscle size too.
Great products which I will use over and over again! Very pleased.
Kind regards,
Michael
Hello everyone
I would like to share my personal experience with SARMS to be more precisely the experience was only with SARMS made from enhancetech.
I started to take SARMS around 20/nov/2020. In the beginning I was bulking and it gave me a lot of strength, stamina and power during the workout session, I was into and RAD140, LGD-4033 and YK11 .
Then I moved to cut using MK-677 and RAD140. Was around 80 days with this cycle and it worked greatly. I would like to share bellow my before and after picture.
Igor Buracof
Igor on the beach today
BEFORE
AFTER
The current pharmaceutical options such as lorcaserin have clearly not been an adequate solution to problem of obesity. Extreme measures such as surgery, mitochondrial decouplers, tapeworm ingestion and illegal stimulants are not discussed.
While weight gain may be caused by medical conditions that alter water balance, commonly the weight gain is understood as accumulation of fatty tissue. Fatty tissue is caused by excess energy intake and deficit of energy expenditure (production of work, production of heat and bypass). In a biological system, such as a human, the energy intake is regulated first by availability, then by appetite and finally, by bioavailability of energy sourches such as fat, sugar, alcohol and protein. Assuming that food as an energy source is available, the energy intake is mainly regulated by appetite unless there is an overt mechanism that causes loss of energy sources, such as digestion disorders.
At the fundamental, biochemical level, there are certain biomolecules that increase or decrease appetite. Originating from the gut, Ghrelin is the primary hormone that creates sense of hunger [1] while, also originating from the gut, anorectic hormone peptide YY3-36 (PYY), cholecystokinine (CCK) and glucagon-like peptide-1 (GLP-1) reduce the appetite in response to energy intake and reduce reward to food intake in the responsible brain parts. Bile acids have an important role: these stimulate PYY and GLP-1 as well as modulate gut microbiota, which participates in appetite regulation in the one hand and energy accumulation efficiency in the other hand [2].
Fatty tissue, by default, “should” inhibit food intake by signalling via leptin and insulin that no more energy is necessary. However, due to cultural pecularities of food overconsumption in certain geographical regions especially, metabolic syndrome may be acquired. Metabolic syndrome is characterized by resistance to insulin (and probably leptin), and it is a risk factor for cardiovascular diseases and type 2 diabetes [3]. Insulin and/or leptin resistance destroys appetite control. Hence, obese people may feel hungry, probably against both their better judgement and superfluous energy reserves.
Food has hedonic reward, taste influences food intake. Food industries and art of culinary have been competing to produce as tasty foods as possible for generations. Children like sugar, for example. Considering these preferences, it is probably no wonder that corn flakes, former healthy food, has become sweeter and sweeter during course of the history [4]. In the same time, in some areas with well-entrenched healthier cuisine, such as Japan, do not experience obesity epidemic to an extent comparable to, for example, USA or Saudi Arabia. Technically, it is not even an addiction [5], and sugar preference is used in animal studies of a marker of normal enjoyment [6] despite having some traits that are sought to identify addictive substances such as dopamine and endorphin release in pleasure center of the brain [7]. While classifications may be of great academic interest, the desire to consume sweets may be comparable to desire to addictive substances and this clearly identifies it as an practical problem. It must be solved lest the situation be determined by rather hard-wired appetite and competition of capitalist food industry[8]. However, tastes can be acquired – for example when a child becomes accustomed to healthy food, that child develops a a preference for healthy food (reviewed in [1]). Taken that into account, the aquired taste of obesity-causing food is the major interventable culprit of obesity behind “junk food” eating cultures that can be identified from the world obesity maps readily available with the help of online search engines. Indeed, genetics plays a part, about 20% according to a huge population based genome-wide population study [9]. It is known that the americans of japanese origin have above-average rates of diabetes in USA [10]. Japan has experienced infiltration of western-like foods such as instant noodles to everyday diet of the japanese, and now the prevalence of type II diabetes or glucose resistance in Japan is 13.5% [11]. However, in Japan people tend to walk instead of driving, eat different foods and do not accept obesity as ‘normal’, and rate of their obesity is much lower than everywhere else in the world. Hence, the nutritional solution is exercise combined with diet of Japan 1975 (it was the maximally healthy one according to analysis) [12]. While the debate about the superiority of low-fat or low-carb diet is continuing in mainstream media, in the scientific literature the debater is more or less over. Low-carb diet and Mediterranean diet are clearly superior to low-fat approach [13], far superior.
Pharmaceutical solutions are at best secondary, unclear at worst. Surgery is the last resort. There are certain other add-on interventions provided by cosmetic industry but these, too, are supplementary. The primary interventions are exercise and diet. The supremacy of (A) traditional Japanese diet, (B) low-carb diet (see also ketogenic diet) and (C) traditional Mediterranean diet are established and most likely, must be part of the solution.
[1] https://pubmed.ncbi.nlm.nih.gov/28229538/
[2] https://pubmed.ncbi.nlm.nih.gov/28356427/
[3] https://pubmed.ncbi.nlm.nih.gov/24582089/
[4] https://www.diabetes.co.uk/blog/2015/03/sugar-in-cereal-who-are-the-worst-offenders/
[5] https://pubmed.ncbi.nlm.nih.gov/27372453/
[6] https://rndb.clps.brown.edu/task/sucrose-preference-test/
[7] https://pubmed.ncbi.nlm.nih.gov/20648910/
[8] https://pubmed.ncbi.nlm.nih.gov/23719144/
[9] https://pubmed.ncbi.nlm.nih.gov/25673413/
[10]https://pubmed.ncbi.nlm.nih.gov/27169694/
[11]https://pubmed.ncbi.nlm.nih.gov/19795421/
[12]https://pubmed.ncbi.nlm.nih.gov/30170306/
[13]https://pubmed.ncbi.nlm.nih.gov/18635428/
[14]https://pubmed.ncbi.nlm.nih.gov/30170306/
Hordenine is a naturally-occurring atypical stimulant that is found in barley, bitter orange and cacti such as Echinopsis candicans. Sometimes it is found in weight loss or athletic performance enhancement supplements in larger amounts and sometimes it is found in fake “bitter orange extracts”, which may actually be a mixture of different synthetic phenylethylamine stimulants [1]. Is hordenine a good enhancer of coffee or a good alternative to it? Indeed, in the first place it is not very well researched. It is one of the many atypical minor phenylethylamine stimulants that is considered reasonably safe in smaller doses. In higher doses, is also sold as a supplement for weight loss or athletic performance enhancer. Are there any concerns?
Hordenine is no doubt bioactive. It is a relatively poor but selective inhibitor of monoamine oxidase B that breaks down dopamine [2] and phenylethylamine (PEA), prolonging their effect in the brain, heart and kidneys. While it does not mimic noradrenaline itself, it inhibits the removal of noradrenaline from synapses, and thus increases noradrenergic tone [2]. Therefore, it is a stimulant. Inhibiting breakdown of dopamine might reduce oxidative stress and might be useful for some neural conditions (mood disorders, Parkinson’s disease) and potentially disadvantageous in others (schizophrenia, anxiety disorders). Inhibition of noradrenaline uptake may be useful in the context of mood and attention disorders while it is reasonable to speculate that it may be dangerous in the context of hypertension and related diseases as well as anxiety disorders. The combined effect of these with other stimulants with different mechanisms may be greater than sum of their parts, and thus more potent as well as more dangerous.
It has been found that hordenine blocks synthesis of melanin, which is a molecule that protects the skin from the damaging effects of the sunlight [3]. The paper discussed that this property of hordenine might have potential pertinent to hyperpigmentation disorders. In the same time, it seems wise to consider that inhibition of normal tanning might increase the risk of skin cancer in some contexts.
An animal study has found that hordenine may be a kidney-friendly substance in mice with chemically induced diabetes. More specifically, hordenine reduced inflammation mediators IL-1beta and IL-6 as well as (in this context) harmful tissue remodeling enzyme MMP-9 [4]. Reduction of oxidative stress indicates normalization of haywire metabolism in the kidneys (ROS). While this is just one study made in animals, it is of great interest because it is not so easy to find molecules that are beneficial for kidneys (or liver).
High doses of hordenine have been investigated in the horse [5]. The responses of the horses were flehmen response (expression of intestinal discomfort, probably), defecation within 60 seconds, respiratory distress and doubling of heart rate. These responses to 2 mg/kg injection were transient and animals biological signs returned to normal within 30 minutes. When the same dose was given to animals orally, no such responses were recorded; the concentration of hordenine returned to baseline within 24 h.
Hordenine reduces the disease causing capacity of certain Pseudomonas aeruginosa or Serratia marcescens strains [6,7]. These bacteria are not so often found from healthy persons. It is unknown whether hordenine has any useful or harmful effect on the healthy persons’ beneficial bacteria that are mostly quite different from these two species.
Hordenine has weak dopamine D2 agonist properties. Consumption of beer is insufficient source of hordenine for this to become pertinent but higher doses found in food supplements with high concentrations might [8]. D2 receptor is pertinent for goal maintenance during mental tasks [9], less receptors are linked to better working memory and task switching.
While increased dopaminergic tone via MAO B inhibition might be beneficial for cognitive enhancement, substantial activation of D2 receptors might reduce cognitive performance, instead. Therefore, while it is clear that hordenine is a cardiovascular, nervous system and metabolism stimulant, nootropic properties are debatable – while it might me mildly nootroopic, the opposite may be true, instead.
[1] https://pubmed.ncbi.nlm.nih.gov/32497396/
[2] https://pubmed.ncbi.nlm.nih.gov/2570842/
[3] https://pubmed.ncbi.nlm.nih.gov/23768344/
[4] https://pubmed.ncbi.nlm.nih.gov/29775900/
[5] https://pubmed.ncbi.nlm.nih.gov/2269269
[6] https://pubmed.ncbi.nlm.nih.gov/29353476/
[7] https://pubmed.ncbi.nlm.nih.gov/30609368/
[8] https://pubmed.ncbi.nlm.nih.gov/31984737/
[9] https://pubmed.ncbi.nlm.nih.gov/30125286//
Recently, a study has been published that considers testosterone restoration as an alternative to testosterone replacement. In aging male, the testosterone levels become lower but generally support sufficient testosterone levels. However, the low-normal levels of testosterone have been associated (causation not implied) with higher levels of mortality, about 35% all-cause mortality [2].
Human Corion Gonadotrophin (HCG) is a powerful hormone that can, in low doses, restore testosterone production but it has caused reduction of testicular volume and fertility parameters [1]. It has been to restore testosterone production of steroid abusers. In otherwise healthy men with low testosterone (<420 ng/dL-1) did not show expected increas in strength but caused significant reduction of testicular volume, gonadotrophin levels and, in a few cases, nipple tenderness. However, improved lean body mass was observed. Hence, long-term use of HGC therapy comes with significant side effects.
Antiestrogens such as clomiphene citrate (CC) counteracts effects of estrogens that give negative feedback to production of upstream sex hormones that promote production of testosterone [1]. Indeed, CC restored levels of follicles stimulating hormone FSH, luteinizing hormone LH and gonadotropin releasing hormone GnRH. While CC has consistently restored production of testosterone, effects on fertility and semen parameters have been variable, especially in older men were refractory to hormone manipulation while younger men had side effects of decreased libdo, lack of energy, decreased sports performance and worse mood.
Third group of anti-estrogenic treatment that aims to restore testosterone levels are aromate ihibitors AI such as anastrozole and letrozole. Since these drugs do not eliminate production of estrogens in men completely, these drugs are unlikely to cause osteoporosis in men. AI are more effective in raising testosterone levels than transdermal forms of testosterone such as testosterone gel [1]. The side effects of AI are minimal, mainly limited to unalarmingly modest increase of prostate specific antigen PSA (biomolecule used assess prostate pathology).
Fourth group is SARMs [3] or selective androgen receptor modulators such as ostarine, a “field leader”. Ostarine support smuscle growth and does not affect or even suppresse prostate growth, and does not significantly suppressing endogenous androgen production in clinically used doses. However, the selectivity of SARMs is not absolute, potency and selectivity appears to be a trade-off. A potent SARM such as ligandrol suppresses endogenous testosterone and also high density cholesterol – these side effects resembe side effects anabolic steroids [4]. SARMS can be expected to have cognition preserving results, some very low (cell culture) level studies with SARMS such as RAD-140 and NEP20 appear to support the theory [5,6].
Finally, some herbal medicines can improve aspects of androgen deficiency. Tribulus terrestris has been reviewed thorouhghly but with mainly positive effects in focus [7]. T. terrestris increases sex drive, appears to have properties that protect heart and blood vessels as well as nervous system from insults, has anti-inflammatory properties. Hovever, the abilities of tribulus terrestris to inreace endurance in rodents could not be replicated in controlled studies with human subjects [8,9]. Eurycoma longifolia is a herbal supplement with respectable traditional use with drawback of relatively high price, widespread distribution of fake extracts, and low bioavailability (10%) of main constituent eurycomanone (tested in rodents). Eurycoma longifolia has been reviewed comprehensively, and it has been tested in humans, mostly in association with aphrodisiac properties[10]. While E. longifolia has not been to subject of thorough exercise research, it seems to modestly improve testosterone levels, fertility parameters and libido on men with late onset hypogonadism, with additional benefits of being anti-diabetic, promoting bone strength and reducing anxiety.
[1]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4650464/
[2]https://pubmed.ncbi.nlm.nih.gov/25041142/
[3]https://pubmed.ncbi.nlm.nih.gov/22459616/
[4]https://pubmed.ncbi.nlm.nih.gov/22459616/
[5]https://pubmed.ncbi.nlm.nih.gov/24177288/
[6]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3959610/
[7]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5503856/
[8]https://pubmed.ncbi.nlm.nih.gov/17530942/
[9]https://pubmed.ncbi.nlm.nih.gov/10861339/
[10]https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6274257/
Chemicals that are designed for one particular purpose can have unexpected side effects – often adverse, sometimes useful. For example, according to anecdotal evidence one of the SARMs (that is not even scientifically tested in humans) can tint the vision green or yellow. However, it is not the side effects of SARMs this post will be about. This post is about current coronavirus COVID-19 or SARS-2 (Severe Acute Respiratory Syndrome 2), a very close relative of coronavirus that caused SARS, and somewhat less close relative to very lethal MERS (Middle East Respiratory Syndrome) and research pertaining to possible treatment.
As concerns the coronaviruses, chemical informatics has revealed that a molecule that has been designed as a SERM (selective estrogen receptor modulator) could be repurposed as a medicine against novel coronavirus [1]. Of course, a computer analysis is not comparable to the rigour of actual human study but the model seems to be legit. Some other molecules found by informatics approach include emodin that has been found as a drug candidate in an earlier study [2]. Emodin is not a SARM, though, it is principally a a molecule that is responsible for laxative and estrogenic properties of certain medicinal rhubarb species. Of note, also melatonin was a „hit” in the analyses that matched coronavirus against the drug database. No experimental data on melatonin and coronavirus was found from scientific literature, though. Nevertheless, in the melatonin is considered as a potential treatment in another white paper [3] and one of the potential mechanisms might be that melatonin does not allow the COVID-19 to kill off the hosts’ T-cells so easily [4]. It seems likely that elderberries may have the same mechanism combating the upper respiratory tract viruses [5]. The other effect of melatonin that may facilitate the favourable income include protection from reactive nitrogen species. Indeed, in addition to direct antiviral mechanisms, immune stimulation and immune stimulant drugs [6] are also considered, and the most promising one, interferon beta-1 peptide is indeed a working solution against coronavirus, and included into medical guidelines [7]. It is known that lack of interferon beta is responsible for lethal pneumonia [8], which is the key difference between serious and non-serious coronavirus infections.
MERS (Middle East Respiratory Syndrome) coronavirus was tested against several drugs. In that study, a drug against malaria, chloroquine, and a drug against parasites, nitazoxanide, also had a „side effect” against the virus that caused MERS, and these two were more than order of magnitude more selective and potent (in vitro, at least) against MERS than most of the antiviral drugs that are used in the hospitals against COVID coronavirus now [9]. Lately, chloroquine has been added to several treatment guidelines, and the United Kingdom banned the export of chloroquine [10]. A now rather uncommon drug that was formerly used to treat arthritis, indomethacin was very effective in treating both SARS and dogs’ coronavirus in dogs [11] and there is an impressive list of potential molecules that could help against coronavirus in the very earliest research phase [12].
Finally, a list of food supplements has been published that has been suggested to ameliorate respiratory tract infections caused by RNA viruses such as influenza and coronavirus in general [13]:
Substance Dose
Ferulic acid 500-1000 mg
Lipoic acid 1200-1800 mg (in place of ferulic acid)
Spirulina 15 g (or 100 mg PCB)
N-Acetylcysteine 1200–1,800 mg
Selenium 50-100 mcg
Glucosamine 3,000 mg or more
Zinc 30-50 mg
Yeast Beta-Glucan 250-500 mg
Elderberry 600–1500 mg
[1] https://www.ncbi.nlm.nih.gov/pubmed/32194980
[3] https://www.sciencedirect.com/science/article/pii/S0024320520303313
[4] https://onlinelibrary.wiley.com/doi/full/10.1046/j.1600-079X.2003.00105.x
[5] https://www.ncbi.nlm.nih.gov/pubmed/31560964
[6] https://www.ncbi.nlm.nih.gov/pubmed/32205350
[7] https://www.ncbi.nlm.nih.gov/pubmed/32164424
[8] https://www.ncbi.nlm.nih.gov/pubmed/26867177
[9] https://www.nature.com/articles/s41422-020-0282-0
[10] https://www.gov.uk/government/publications/medicines-that-cannot-be-parallel-exported-from-the-uk
[11] https://www.ncbi.nlm.nih.gov/pubmed/17302372
[12] https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4195804/
[13] https://www.ncbi.nlm.nih.gov/pubmed/32061635