Needtogetaas. My take on Ketotifen.



Ketotifen is a second-generation noncompetitive H1antihistamine and mast cell stabilizer with a half life of around 12 hours. Due to its antihistiamine properties, it will bring down regulation of the beta receptors to a halt which we delve into more eventually. It is most commonly sold in as a salt of fumaric acid, ketotifen fumarate, and is available in two different deliveries. We as weekend warriors want to use its oral form, which is used to prevent asthma attacks. Side effects include drowsiness, weight gain, dry mouth, irritability, and increased nosebleeds, appetite, change, diarrhea, chills, increased sweating and insomnia. (

Ketotifen Inceases LBM

Individuals with wasting syndrome lose muscle aka lean body mass rather than body fat which is due to the lack of anabolic hormones in their body. Several possible alternatives to the approved drugs for AIDS-related wasting are discussed, one of them being Ketotifen. TNF inhibitors prevent inflammation from causing diseases such as Chron’s disease. As a reminder, inflammation is the biggest cause of all diseases. TNF-inhibitors also increase hunger as a decrease inflammation tends to lead in an increase in metabolic rate. This would make perfect sense since an elevated metabolic rate is associated with a healthy immune system. A study combining ketotifen and oxymetholone, the oral anabolic steroid, was presented at the Ninth International AIDS Conference. Preliminary data from a study combining ketotifen and oxymetholone showed that 18 out of 22 patients gained an average of 11.4 pounds after treatment of an average of 3.9 weeks. Sure it was not ketotifen alone, but considering their state of condition, it sure did not counter the effects of oxymetholone.  (Smart T. GMHC Treat Issues. 1995 May;9(5):7-8, 12.)


Ketotifen may prove as another form of HRT

The aim of this study I came across was to identify the sites of the inhibitory action of TNF-alpha (tumor necrosis factor alpha) on LH/hCG injections-stimulated testosterone formation. By using cultured porcine Leydig cells as a model, TNF-alpha was shown to inhibit testosterone secretion when testicular cells were stimulated with hCG but not when incubated with 22R-hydroxycholesterol (a cholesterol substrate derivative that readily passes through cell and mitochondrial membranes). Such an observation suggested that the cytokine may affect cholesterol transport and even the availability to cytochrome P450scc in the mitochondria. Specifically, we report here that TNFalpha reduced in a dose- and time-dependent manner hCG-induced StAR (steroidogenic acute regulatory protein) levels. The maximal and half-maximal effects were obtained with 20 ng/ml and 1.6 ng/ml of TNFalpha, respectively. Maximal inhibitory effects of TNFalpha on StAR messenger RNA and protein levels were obtained after 48 h of treatment. Additionally, the presence of TNFalpha receptors P55 in terms of protein (identified through cross-linking experiments) and messenger RNA (identified through RT-PCR analysis) suggested that the effects of the cytokine are directly exerted on the testicular steroidogenic cell type. So in essence TNF alpha as it rises lowers levels of testosterone. Since, ketotifen is a TNF alpha inhibitor; it may indirectly increase testosterone levels quite substantially; especially if one may be at stake for waste syndrome.  (Mauduit C, Endocrinology 1998 Jun;139(6):2863-8)


I am going to take it one step further and show documentation of a study in which testosterone injections LOWERED levels of TNF alpha in hypogonadal men. Testosterone has immune-modulating properties, and current in vitro evidence suggests that testosterone may suppress the expression of the proinflammatory cytokines TNFalpha, IL-1beta, and IL-6 and potentiate the expression of the anti inflammatory cytokine IL-10. That is not to say that testosterone does not suppress the Immune system. When testosterone gets to high the body starts to produce less auto immune hormones to make more anabolic hormones. Back to the study; researchers reported a randomized, single-blind, placebo-controlled, crossover study of testosterone replacement in the form of Sustanon 100 vs. placebo in 27 men ranging in age from 53 to 71 years old with low levels of total and free testosterone. When the men were injected with testosterone, levels of TNF alpha and IL-1 beta dropped notably.  Levels of cholesterol had also dropped significantly which shows the heart protective properties of keeping TNF-alpha under control. In conclusion, testosterone replacement shifts the cytokine balance to a state of reduced inflammation and lowers total cholesterol. Twenty of these men had established coronary disease, and because total cholesterol is a cardiovascular risk factor, and pro inflammatory cytokines mediate the development and complications associated with atheromatous plaque, these properties may have particular relevance in men with overt vascular disease. Another reason why a study in the future should be done on Ketotifen and its affects on sex hormones, I predict good things to come from a study of that kind. If you ask me, I will tell you it’s one heck of a drug and should be used in pct, not only because of its positive effects on testosterone but also IGF-1 which we will get into next. (Malkin CJ J Clin Endocrinol Metab. 2004 Jul;89(7):3313-8.)


In this study, Conscious rats were injected intravenously with recombinant human TNFalpha or vehicle for 24 h. TNFalpha decreased the concentration of both total and free IGF-I in the plasma by 30-40%. This change was associated with a reduction in IGF-I mRNA expression in liver by 39%, gastrocnemius by 73%, soleus by 46% and the heart by 63%, but a 2.5-fold increase in the whole kidney. What I found interesting was that TNFalpha did not alter IGF-II mRNA expression in skeletal muscle. TNFalpha also increased IGFBP-1 in the blood (4times-fold) and this response was associated with an increase in IGFBP-1 mRNA expression in both liver (3times-fold) and kidney (9times-fold). However, IGFBP-3 levels in the blood were reduced 38% in response to the injection of TNFalpha. This change was accompanied by a 60-80% reduction of IGFBP-3 mRNA in the liver and kidney but no significant change in muscle. Hepatic mRNA levels of the acid-labile subunit were also reduced by TNFalpha by 46%. Finally, tissue expression of mac25 (also referred to IGFBP-related protein-1) mRNA was increased in gastrocnemius by 50% but remained unchanged in the liver and kidney. These results more fully characterize the changes in various elements of the IGF system and, thereby, provide potential mechanisms for the alterations in the circulating IGF system as well as for changes in tissue metabolism observed during catabolic insults associated with increased TNFalpha expression. As you see the same applies to IGF-1, the more the TNF alpha the less available IGF one will have. When a TNF inhibitor is presented, IGF levels will rise. (Lang CH Growth Horm IGF Res 2001 Aug;11(4):250-60)

Ketotifen may have anti-catabolic properties

When individuals train hard, TNF alpha has been shown to rise. Of course we know that if you were to take ketotifen post training it would not be as great as prior to training but that is still fine. Caffeine in moderate doses is shown to increase performance yet keep cortisol lower compared to those who train without it. I simply suggesting that taking Ketotifen prior to training like most do will still provide the intended anti-catabolic effects that I theorize about. As I mentioned before, we need more studies done with ketotifen especially regarding its effects on the endocrine system. (Pedersen BK et. al. Exerc Immunol Rev 2001;7:18-31)


Ketotifen aids in easing Irritable Bowel Syndrome

Mast cell activation is thought to be involved in visceral hypersensitivity, one of the main characteristics of the irritable bowel syndrome (IBS). A study was therefore undertaken to investigate the effect of the mast cell stabiliser ketotifen on rectal sensitivity and symptoms in patients with IBS. 60 patients with IBS underwent a barostat study to assess rectal sensitivity before and after 8 weeks of treatment. After the initial barostat, patients were randomized to receive ketotifen or placebo. IBS symptoms and health-related quality of life were scored. In addition, mast cells were quantified and spontaneous release of tryptase and histamine was determined in rectal biopsies and compared with biopsies from 22 age- and gender-matched healthy volunteers. Ketotifen but not placebo increased the threshold for discomfort in patients with IBS with visceral hypersensitivity. This effect was not observed in normosensitive patients with IBS. Ketotifen significantly decreased abdominal pain and other IBS symptoms and improved quality of life. The number of mast cells in rectal biopsies and spontaneous release of tryptase were lower in patients with IBS than in healthy volunteers. Spontaneous release of histamine was mostly undetectable but was slightly increased in patients with IBS compared with healthy volunteers. Histamine and tryptase release were not altered by ketotifen. This study shows that ketotifen increases the threshold for discomfort in patients with IBS with visceral hypersensitivity, reduces IBS symptoms and improves health-related quality of life. Whether this effect is secondary to the mast cell stabilising properties of ketotifen or H(1) receptor antagonism remains to be further investigated. (Gut. 2010 Sep;59(9):1213-21. Epub 2010 Jul 21.)

Combining Ketotifen with other agents

Due to ketotifen’s beta receptor upregulating properties, can be used as aid to one’s clenbuterol cycle. After a week or two on Clen, your beta 2 receptors will be saturated and down regulated. ketitofen will prevent this and even increases fat loss with its upregulating effect on the beta 3 receptors. You can take less of Clen while on ketotifen as well, since ketotifen will increase clen’s effectiveness by a third.

Taking ketotifen with ephedrine is pretty synergistic, as ephedrine works highly upon beta 3 receptors, ketotifen upregulates those beta receptors, thus making it more potent. Plus the fact that it reduces the amount you need for these agents, will in turn reduce the amount of side effects. IF you have the experience and tolerance, stacking all three of these agents would be a tremendous thermogenic fat burning stack.

I recommend taking 1mg of ketotifen 30 minutes prior to a meal twice a day. Remember take it while on clen or ECA to keep the receptors clean and maximize those cycles.


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