To be hard, you need to get HARD. It's that simple.
Core HARD is the pinnacle in recomposition supplementation. The ingredients in HARD have been specifically chosen to balance your hormonal environment and maximize your lean mass.
- 3 capsules per serving.
- 28 servings per container.
- Body recomposition.
Your diet is impeccable and couldn’t be any more in check – macros, micros, you have it all down. Your workouts? Get out of here! You have slaved, grinded, and grunted your way through leg workouts so intense the gym staff cried – and those were on your worst days. And yet, something is missing.
It’s that “extra” level of shred, “that look.” You know exactly what we mean. That type of leanness and density that makes an arm look twice as big, a stomach look twice as lean, and a forearm look like a roadmap for the Italian countryside. It’s that kind of elusive hardness that’s so rare, most of us simply chalk it up to genetics, or luck, or steroids, or whatever excuse we have handy – and yet we all still want it.
The reality? It isn’t all that unattainable. Getting “that” look, “that” hardness, is about balance and recomposition. It’s a matter of adding in that final piece of the puzzle that makes the entire picture come out perfectly.
To be hard, you need to get HARD. It’s that simple.
Core HARD is another product in the Core Nutritionals’ lineup to follow the basic, but indispensable principles that Core Nutritionals is slowly making an industry standard: create products with effective ingredients, in effective doses, in a non-proprietary formula. This time around, we have applied those principles to the problem of softness that we all despise and have developed the most advanced ultra-hardening and recomposition agent on the market.
Taking advantage of both the old and the new, Core Nutritionals has employed both modern, cutting-edge compounds and traditional herbs to create a balanced approach to delivering hardness. Key ingredients in Core HARD affect some of the body’s critical physiological pathways, combining sexiness and science in a single, non-proprietary formula. We have included five powerful ingredients into a full month's worth of stimulant free, recomposition goodness.
Core HARD can be used alone, or in a stack with other Core Nutritionals’ products. The BURN HARD stack (Core HARD plus Core BURN) will be the ultimate fat blasting and hardening stack. Men can try the HARD A.B.s stack (Core HARD plus Core ALPHA plus Core BURN)to help create that chiseled look that all men want.
Phosphatidylserine, colloquially known as PS, is a nearly ubiquitous phospholipid found in various membranous tissues throughout the body. PS’s ubiquity coincides with its necessity for crucial physiological functions, as the phospholipid is implicated in several components of cell communication, as well as the mediation of catecholamine synthesis and transmission in the brain (along with other neuroendocrine functions). In a fitness-related context, a nascent but growing body of methodologically-sound research suggests that PS may play a role in increasing exercise capacity.
Studies administering the compound in both acute and chronic fashion suggest that PS has a measurable effect on exercise capacity. In a double-blind, placebo-controlled, randomized trial involving 16 trained athletes, phosphatidylserine was administered for 10 days prior to an acute exercise challenge. Exercise markers such as exercise time to exhaustion, sprint performance, and ratings of perceived exertion, were measured post-exercise. The authors found that exercise time to exhaustion was significantly altered. Related studies using similar serving sizes have found that chronic PS administration increased shot accuracy in golfers, increased exercise time to exhaustion by 28% in cyclists, and reduced subjective feelings of stress and soreness in others.
Overall, phosphatidylserine appears to play a valuable role in the increase in exercise capacity. PS may therefore play a critical role in the continued exercise success of bodybuilders in a, “cutting” or recomposition stage.
KSM-66® Full-spectrum Ashwagandha root extract (5% Withanolides)
Withania somnifera Dunal, colloquially known as Winter Cherry or Indian Ginseng, is an herb that features prominently in the traditional Indian medicinal system of Ayurveda. Known as Ashwagandha in Ayurveda, Withania somnifera is a critical ingredient in various Ayurvedic tonics and tinctures prepared as a traditional remedy for the treatment of various ailments.
Recently identified as a potent adaptogenic and target for therapeutic applications, Ashwaghanda has been the subject of numerous animal, pre-clinical, and clinical trials designed to examine its potential effects as an antioxidant, anti-carcinogenic, anxiolytic, antibacterial, antifungal, and immonumodulating compound. Ashwaghanda’s broad therapeutic potential is hypothesized to be the result of its robust phytochemical profile, including a wide swath of alkaloids, sitoindosides, and the highly biologically active withanolide group. As the principally biologically active compounds within Ashwaghanda, withanolides such as withanone, withaferine A, withanolides A, D, and G have been identified, isolated, and extensively studied in the various applications noted above.
In recognition of the potential physiological benefits of withanolides, Core Nutritionals selected KSM-66® to include in its HARD formula. KSM-66® is a full-spectrum Ashwaghanda extract, standardized for 5% withanolides – meaning that KSM-66® not only includes the full range of biologically active compounds within Ashwaghanda, but also that it contains the highest currently available concentration of the principally active withanolides (5%).
The high concentrations of withanolides within KSM-66® has resulted in encouraging results in a number of human, clinical trials – particularly considering many of these trials were conducted using the methodological gold standard of randomization, double-blind delivery, and placebo control. Amongst the most impressive results contained in these trials:
- A 27.9% reduction in serum cortisol levels, measured over 60 days in a trial featuring 64 chronically stressed adults.
- Statistically significant increases to endurance and stamina, as measured by VO2 max, in a clinical trial featuring 50 healthy, exercise-trained adults.
- Increased measures of well-being as reported by self-assessment scales, included in both the clinical trials mentioned above.
- Statistically significant increases in serum testosterone levels in a clinical trial featuring 68 infertile men.
Though each of these results is impressive, perhaps the most significant is the 27.9% reduction in cortisol seen in the 60 day trial. As detailed above, cortisol possesses a multitude of potentially degradative physiological effects, including: inhibiting glucose uptake, causing a constriction of the vasculature (vasoconstriction), the breakdown of glycogen, and inarguably the result most would desire to avoid, proteolysis (the breakdown of muscle tissue).
To put it the simplest way possible, cortisol’s chief functions involve either turning on, or shutting off, the very things we as fitness enthusiasts want to avoid or turn on, respectively!
N-Coumaroyldopamine is a natural analogue to the phytochemical N-Caffeoyldopamine, itself found prominently in various plants, including cocoa (Theobroma cacao L.). N-Coumaroyldopamine, its parent compounds, and other analogs that derive from its parent compound, have recently been the subject of phytochemical analyses due to their chemical similarity to sympathomimetic amines known to couple to the beta-2-adrenergic receptor.
Phytochemical analyses were subsequently designed to assess the potency of N-Coumaroyldopamine and N-Caffeoyldopamine as beta-2-adrenergic receptor agonists – or, in simpler terms, their ability to “turn on” the fabled beta-2-adrenergic receptor. In these trials, the phytochemicals were shown to be as potent as several well-known beta-2-adrenergic receptor agonists (salbutamol, procaterol, and fenoterol). You read that correctly: N-Coumaroyldopamine and N-Caffeoyldopamine were found to bind as tightly to the beta-2-adrenergic receptor as well known synthetic compounds!
The desirability of activating the beta-2-adrenergic receptor arises due to the critical role that beta-2-adrenertic receptors play in both skeletal muscle and fat metabolic function. In particular, beta-2-adrenergic receptors have been shown to induce dilation in the vasculature (vasodilation – the process involved in a “pump”), increase oxygen uptake and nutrient transport to skeletal muscle, regulate thermogenesis (the production of body heat), inhibit the pro-adipogenic (fat constructing) effects of other adrenergic receptor types, as well as directly increase lipolysis and the oxidation of fatty acids – the literal burning of fat tissue.
Beta-2-adrenergic receptors achieve these effects via one of the body’s key chemical messengers, known as cAMP (cyclic adenosine monophosphate). cAMP works as a sort of cell-type translator and foreman: it receives an input from, say, a receptor such as the beta-2-adrenergic receptor, and then communicates and directs the types of cells that the beta-2-adrenergic receptor would like to target.
Just within the context of beta-2-adrenergic agonism, this amounts to cAMP increasing resting metabolic rate and caloric expenditure (the amount of calories you burn), improving peripheral sensitivity to glucose and glucose utilization, reduction of gluconeogenesis, induction of AMPk (adenosine monophosphate kinase) release, triggering of lipolysis (the literal burning of fat tissue we spoke about earlier), the inhibition of lipogenesis (the creation of fat tissue), and vasodilation.
Or, in other words, cAMP is involved in nearly every beneficial physiological process that a lifter, runner, hiker, jumper, runner, tumbler, and fumbler would want. cAMP is involved in:
- Increasing bloodflow (“pump”).
- Reducing muscle protein usage (catabolism).
- Increasing muscle protein synthesis.
- Increasing adipose utilization.
To say that cAMP is a desirable compound to increase the release of – which activating the beta-2-adrenergic receptor does – would qualify as the understatement of the year!
What we typically refer to as “Estrogen,” is in fact a group of three biologically distinct hormones – estradiol (E2), estrone (E1), and estriol (E3), each possessing different activities in different cell, tissue, and receptor types. When experts refer to either the benefits or downfalls of “estrogen," they really mean to (but probably cannot) identify a specific estrogen.
These specific estrogens, in turn, metabolize into even more specific estrogen sub-compounds, such as the 2-hydroxyestrogens (2-OHE’s), 2-methoxyestrogens, 16a-hydroxyestrone (16-OHE1), and 4-hydroxyestrogens (4-OHE’s). As their parent estrogens, these estrogen metabolites exert different effects depending upon the tissue and cell one is examining. In fact, two estrogen metabolites in particular, 16-OHE1 and 2-OHE, have such contrasting cellular activities that 2-OHE is an estrogen antagonist. Yes, that is correct: there is an anti-estrogen, estrogen.
In recent years, so-called “phytonutrients” have become the focus of clinical research, as these natural compounds have shown the ability to increase the ratio of good, estrogen decreasing estrogens (such as 2-OHE), to bad, estrogen increasing estrogens (such as 16-OHE1). One of these phytonutrients, a dietary indole known as indole-3-carbinol (I3C), is the bioactive phytochemical and a presumed modulator of reduced cancer risk in areas with high cruciferous vegetable consumption. Unfortunately, despite its potent antiestrogenic activity, I3C is highly molecularly unstable, and therefore unsuitable for use as a therapeutic agent or dietary supplement.
Luckily, however, I3C readily metabolizes into the secondary indole 3,3’ diindolylmethane, or DIM for short. When used in a supplemental fashion in clinical trials, DIM appears to possess all the positive effects of its parent compound with respect to antiestrogenic action – promoting the metabolism of beneficial estrogens that themselves reduce estrogenic activity.
Aside from its healthy-estrogen promoting abilities, DIM also exerts its own direct physiological effects, including:
- Promoting pathways of internal estrogen metabolism that favour the production of anti-estrogen estrogens.
- Adjusting the activity of certain cytochrome enzymes, reducing the activity at the estrogen receptor site.
- Limit the cell division and growth of certain estrogens.
Despite the bodybuilding community’s single-minded crusade to eliminate estrogen wherever it lie in wait, compounds such as DIM show us that estrogen is a very diverse set of compounds – and that we should actively pursue increasing certain estrogens that have beneficial, and ironically, anti-estrogenic effects.
Though the literature surrounding L-theanine is still emerging, the amino acid is slowly building a reputation as one of the most interesting and exciting compounds being targeted for therapeutic use. L-theanine is an amino acid found almost exclusively in tea, constituting approximately 1-2% of the dry weight of tea – resulting in a 25–60 mg theanine load per 200 ml serving of liquid tea.
First identified in green tea and in the mushroom Xerocomus badius, L-theanine readily crosses the blood-brain barrier in a dose-dependent manner, and it is thought to inﬂuence the central nervous system (CNS) through a variety of mechanisms, including:
- Increasing the release and concentration of dopamine.
- Inhibiting glutamate reuptake and blockade of glutamate receptors in the hippocampus.
- Increasing gamma-aminobutyric acid (GABA – a neurotransmitter associated with the regulation of responses) concentrations.
- Increasing levels of serotonin.
In addition to these more well-demonstrated effects, emerging electroencephalography trials on theanine suggest that the amino acid may exert a positive effect on alpha waves – a type of brain wave implicated in restful relaxation. Alpha activity has also been associated with increased creativity, increased performance under stress, and improved learning and concentration, as well as decreased anxiety.
- Kingsley M, Wadsworth D, Kilduff LP, McEneny J, Benton D; Wadsworth; Kilduff; McEneny; Benton (August 2005). "Effects of phosphatidylserine on oxidative stress following intermittent running". Medicine and Science in Sports and Exercise 37 (8): 1300–6.
- Kingsley MI, Miller M, Kilduff LP, McEneny J, Benton D; Miller; Kilduff; McEneny; Benton (January 2006). "Effects of phosphatidylserine on exercise capacity during cycling in active males". Medicine and Science in Sports and Exercise 38 (1): 64–71.
- Jäger R, Purpura M, Geiss K-R, Weiß M, Baumeister J, Amatulli F, Schröder L, Herwegen H; Purpura; Geiss; Weiß; Baumeister; Amatulli; Schröder; Herwegen (December 2007). "The effect of phosphatidylserine on golf performance". International Society of Sports Nutrition 4 (1): 23.
- Starks MA, Starks SL, Kingsley M, Purpura M, Jäger R; Starks; Kingsley; Purpura; Jäger (July 2008). "The effects of phosphatidylserine on endocrine response to moderate intensity exercise". Journal of the International Society of Sports Nutrition 5 (1): 11.
- Monteleone P, Maj M, Beinat L, Natale M, Kemali D; Maj; Beinat; Natale; Kemali (1992). "Blunting by chronic phosphatidylserine administration of the stress-induced activation of the hypothalamo-pituitary-adrenal axis in healthy men". European Journal of Clinical Pharmacology 42 (4): 385–8. doi:10.1007/BF00280123 (inactive 2015- 02- 01). PMID 1325348.
- Fernholz KM, Seifert JG, Bacharach DW, Burke ER, Gazal O (2000). "The Effects of Phosphatidyl Serine on Markers of Muscular Stress in Endurance Runners [abstract]". Medicine and Science in Sports and Exercise 32 (4): S321.
- Bhattacharya SK, Muruganandam AV. Adaptogenic activity of Withania somnifera: An experimental study using a rat model of chronic stress. Pharmacol Biochem Behav 2003;75:547-55.
- Singh G, Sharma PK, Dudhe R, Singh S. Biological activities of Withania somnifera. Ann Biol Res 2010;1:56-63.
- Sharma V, Sharma S, Pracheta, Paliwal R. Withania somnifera: A rejuvenating ayurvedic medicinal herb for the treatment of various human ailments. Int J PharmTech Res 2011;3:187-92.
- Kulkarni SK, Dhir A. Withania somnifera: An Indian ginseng. Prog NeuroPsychopharmacol Biol Psychiatry 2008;32:1093-05.
- Bhattacharya SK, Goel RK, Kaur R, Ghosal S. Antistress activity of sitoindosides VII and VIII, new acylsterylglucosides from Withania somnifera. Phytother Res 1987;1:32-7.
- Ghosal S, Lal J, Srivastava R, Bhattacharya SK, Upadhyay SN, Jaiswal AK, et al. Immunomodulatory and CNS effects of sitoindosides IX and X, two new glycowithanolides from Withania somnifera. Phytother Res 1989;3:201- 6.
- Park, JB. N-coumaroyldopamine and N-caffeoyldopamine increase cAMP via beta 2- adrenoceptors in myelocytic U937 cells. FASEB J. 2005 Apr;19(6):497-502.
- St-Onge. Dietary fats, teas, dairy and nuts: potential functional food for weight control? Am J Clin Nutr 2005 81(1):7-15.
- Kuriyama S et al. Green Tea Consumption and Mortality Due to Cardiovascular Disease, Cancer, and All Causes in Japan The Ohsaki Study. JAMA 2006;296:1255-1265.
- Coimbra S et al. Green tea consumption improves plasma lipid profiles in adults. Nutrition Research 2006;26(11): 604-607.
- Bryan J. Psychological effects of dietary components of tea: caffeine and L-theanine. Nutr Rev 2008;66(2):82-90.
- Nobre AC, Rao A, Owen GN. L-theanine, a natural constituent in tea, and its effect on mental state. Asia Pac J Clin Nutr 2008;17 Suppl 1:167-8.
- Kimura K, Ozeki M, Juneja LR, Ohira H. L-Theanine reduces psychological and physiological stress responses. Biol Psychol 2007;74(1):39-45.
- L-theanine. Monograph. Altern Med Rev 2005;10(2):136-8.
- Dulloo AG, Duret C, Rohrer D, Girardier L, Mensi N, Fathi M, Chantre P, Vandermander J. Efficacy of a green tea extract rich in catechin polyphenols and caffeine in increasing 24- h energy expenditure and fat oxidation in humans. Am J Clin Nutr 1999;70(6):1040-5.
- Hertog MGL, Feskens EJM, Hollman PCH, et al. Dietary antioxidant flavonoids and risk of coronary disease: the Zutphen Elderly Study. Lancet 1993;342:1007-11.
- Keli SO, Hertog MGL, Feskens EJM, Kromhout D. Dietary flavonoids, antioxidant vitamins, and incidence of stroke. Arch Intern Med 1996;156:637-42.
- Duffy SJ, Keaney JF Jr, Holbrook M, Gokce N, Swerdloff PL, Frei B, Vita JA. Shortand long-term black tea consumption reverses endothelial dysfunction in patients with coronary artery disease. Circulation 2001;104:151-6.
- Isemura M, Saeki K, Kimura T, Hayakawa S, Minami T, Sazuka M. Tea catechins and related polyphenols as anti- cancer agents. Biofactors. 2000;13(1-4):81-5.
- Hakim IA, Alsaif MA, Alduwaihy M, Al-Rubeaan K, Al-Nuaim AR, Al-Attas OS. Tea consumption and the prevalence of coronary heart disease in Saudi adults: results from a Saudi national study. Prev Med 2003;36(1):64- 70.
- Sesso HD, Gaziano JM, Buring JE, Hennekens CH. Coffee and tea intake and the risk of myocardial infarction. Am J Epidemiol 1999;149:162-7.
- Meilahn EN. De Stavola B. Allen DS. Fentiman I. Bradlow HL. Sepkovic DW. Kuller LH. Do urinary estrogen metabolites predict breast cancer? Follow up of the Guernsey III cohort. Br J Cancer. 1998;78:1250–1255.
- Schneider J. Huh MM. Bradlow HL. Fishman J. Antiestrogen action of 2-hydroxyestrone on MCF-7 human breast cancer cells. J Biol Chem. 1984;259:4840–4845.
- Telang NT. Suto A. Wong GY. Osborne MP. Bradlow HL. Induction by estrogen metabolite 16 alpha- hydroxyestrone of genotoxic damage and aberrant proliferation in mouse mammary epithelial cells. J Natl Cancer Inst. 1992;84:634–638.
- Ho GH. Luo XW. Ji CY. Foo SC. Ng EH. Urinary 2/16alpha-hydroxyestorne ratio: correlation with serum insulin- like growth factor binding protein-3 and a potential biomarker of breast cancer risk. Ann Acad Med Singap. 1998;27:294–299.
- Zheng W. Dunning L. Jin F. Holtzman J. Urinary estrogen metabolites and breast cancer: a case-control study. Cancer Epidemiol Biomark Prev. 1997;6:505–509.
- Ursin G. London S. Stanczk FZ. Gentzschein E. Paganini-Hill A. Ross RK. Pike MC. Urinary 2- hydroxyestrone/16alpha-hydroxyestrone ratio and risk of breast cancer in postmenopausal women. J Natl Cancer Inst. 1999;91:1067–1072.
- Muti P. Bradlow HL. Micheli A. Krogh V. Freudenheim JL. Schunemann HJ. Stanulla M. Yang J. Sepkovic DW. Trevisan M. Berrino F. Metabolism and risk of breast cancer: a prospective analysis of 2:16 hydroxyestrone ratio and risk of breast cancer in premenopausal and postmenopausal women. Cancer Epidemiol. 2000;11:635–640.
- Tiwari RK. Guo L. Bradlow HL. Telang NT. Osborne MP. Selective responsiveness of human breast cancer cells to indole-3-carbinol, a chemopreventive agent. J Natl Cancer Inst. 1994;86:126–131.
- Sepkovic DW. Bradlow HL. Bell M. Quantitative determination of 3,3′-diindolylmethane in the urine of individuals receiving indole-3-carbinol. Nutr Cancer. 2002;41:57–63.
- Li Y. Wang Z. Kong D. Murthy S. Dou QP. Sheng S. Reddy GP. Sarkar FH. Regulation of FOXO3a/β- catenin/GSK-3β signaling by 3,3′-diindolylmethane contributes to inhibition of cell proliferation and induction of apoptosis in prostate cancer cells. J Biol Chem. 2007;282:21542–21550.
- Rahman KM. Ali S. Aboukameel A. Sarkar SH. Wang Z. Philip PA. Sakr WA. Raz A. Inactivation of NF-κB by 3,3′-diindolylmethane contributes to increased apoptosis induced by chemotherapeutic agent in breast cancer cells. Mol Cancer Ther. 2007;6:2757–2765.