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Luperform Specifications

Warning: contains lupins (allergen)

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Active Components:

  • Powderised lupin standardised for lupin alkaloids including including sparteine, albine, lupanine, lupinine, anagyrine, angustifoline, retamine, calpurnine, matrine, aphylline, cytisine, oxolupanine, sophocarpine, aphyllidine, aloperine, baptifoline, mutiflorine, ammodendrine, and others. 

  • Choline bitartrate

  • Iodine

 

Form:

Luperform comes as an off-white herbal powder to be added at 20mg to 100mg per serve of finished product. This performance ingredient is certified and guaranteed in purity using Fourier Transform (Infra-Red) Raman Spectroscopy. Imparts a bitter, nutty flavour.

 

Recommended Application:

  • 20mg - 100mg per serve of finished product (do not exceed recommendations)

    • Resistance training or endurance training

    • Energy enhancement

    • Anabolic

    • Weight loss

 

Research highlights:

  • COMT Inhibitor

  • MAO Inhibitor

  • Appetite Suppressant

  • Anabolic through GH/IGF-1 Axis

  • Increased contractile force

  • Strength and endurance

  • Increased dopamine and adrenaline

  • Increased lipolysis and decreased desire for low nutrient value foods.  

 

Permissible Label and Advertising Claims Under FSANZ:

  • Necessary for the normal production of thyroid hormones

  • Necessary for normal energy metabolism

  • Contributes to normal fat metabolism

  • Contributes to the maintenance of normal liver function

 

Research Details:

Luperform, (Lupinus spp standardised extract) is the dried, powdered seeds of Lupinus varieties. 

Lupins seeds have traditionally been used medicinally in both Europe and Subcontinental Asia and as a general food stuff (1,2,3,4). Uses have included antibacterial, antifungal, antidiabetic and appetite suppressing activities. 

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The active alkaloids described above are derived from the amino acid lysine, and encompass a wide range of structures and activities (5,6). Many of these molecules have activity at the nicotinic acetylcholine receptors and promote the release of nitric oxide, adrenaline and dopamine. Nitric Oxide is an important anabolic signalling factor (7). While nitric oxide expression in skeletal muscle during exercise leads to a down regulation of contractile force (8), pervading the synaptic cleft with nicotinic acetylcholine receptor agonists (such as those found in luperform) ensures contractile strength is not diminished in a similar manner (9). This may be due to the increase in catecholamine secretion including adrenaline and dopamine but also potentially muscle sparing hormones such as the up-regulated secretion of growth hormone. In fact WADA found an overall 17% performance increase in the highest performing athletes who tested positive for nicotine (10). Nicotine however is a double edged sword in that the negative consequences include addiction, high cost and carcinogenic interaction with Cytochrome P450 superclass-enzyme. 

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It is well known and previously explored that the compound has primary action at the Nicotinic Acetylcholine Receptor (nAChR) (11) which enhances peak physical (12), cognitive performance (13) and lipolytic activity (14). However, the components of Luperform elicit a variety of secondary rejuvenating effects through a number of mechanisms including the ability to induce the release of Insulin, Growth Hormone and IGF-1. 

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The natural alkaloids in Luperform responsible for insulin release include, but are not limited to multiflorine, lupanine, sophocarpine N-oxide, N-methylcytisine, sparteine and epilupanine N-oxide and related compounds and metabolites (as a natural extract the list is extensive) (15). Insulin release as a response to heightened blood sugar levels is significantly enhanced by these compounds (16), even when the insulin producing beta islet cells have sustained DNA damage and under normal circumstances are unable to produce insulin (17).  

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The heightened production of insulin, Luperform on its own has unique and worthwhile benefits, including the potential treatment of diabetes and hyperglycaemia (18). Insulin induces translocation of GLUT-4 (sugar and amino acid transporter protein) in skeletal muscle cells (19) to increase glucose uptake and thus boost energy supply for muscular performance (20). The increased sugar uptake is not limited to muscle and is seen in the cortical regions of the brain where sugar is a primary energy source (21) and used to produce neurotransmitters and to enhance learning and long term memory formation (22). When the frontal cortex experiences heightened glucose transport into cells, acting in synergy with the increased energy requirement as a result of nAChR activation by the lupin alkaloids (23) an increase in cognitive enhancement (24) and a counter to the development of Alzheimer's disease would be expected (25). Heightened insulin levels have also been shown to boost memory and improve mood (26).  

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Many of the alkaloids in Luperform have been found to induce the release of Insulin-like Growth Factor-1 (IGF-1) and Growth Hormone (GH) (27). GH elicits its effects through the release of IGF-1 (28) and causes striated muscle hypertrophy (29). In addition it upregulates gluconeogenesis (30) in the liver supplying glucose utilized by the insulin releasing pathway of Luperform to increase muscle and brain glucose uptake. 

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Importantly, the alkaloids stimulate the activation of lipases in white adipose tissue resulting in the utilisation of fat as an energy source (31). IGF-1 elicits similar effects (often being the primary mediator) to GH (32) and has insulin-like effects brought about by its structural similarity to proinsulin (33). IGF-1 is also an important neurotrophic and neuroprotective hormone, enhancing brain development and neuronal survival and is currently under investigation as a treatment for Alzheimer's disease (34). Moreover it has been identified as an antidepressant (35). The release of GH, and in turn IGF-1 (collectively referred to as the GH/IGF-1 axis) is stimulated by GH releasing hormone (GHRH) and the amount of GH released per unit of GHRH is effectively doubled by moderate cholinesterase inhibition (36). The alkaloids in Luperform which inhibit acetylcholinesterase and butyrylcholinesterase include, but are not limited to anagyrine, ammodendrine, cytisine, and epilupinine derivatives, and these in turn have the effect of releasing GH and IGF-1 (37).  

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References:

1. Bailey, C. J., & Day, C. (1989). Traditional plant medicines as treatments for diabetes. Diabetes care, 12(8), 553-564.

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2. Wazaify, M., Afifi, F. U., El-Khateeb, M., & Ajlouni, K. (2011). Complementary and alternative medicine use among Jordanian patients with diabetes.Complementary therapies in clinical practice, 17(2), 71-75.

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3. Wiedenfeld, H., & Roder, E. (1991). Pyrrolizidine alkaloids from Ageratum conyzoides. Planta Med, 57(6), 578-579.

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4. Jiang Su Xin Yi Xue Yuan, Ed., "Zhong yao da ci dian," Shanghai ren min chu ban she, Shanghai, p. 2135.

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5. Wink, M., & Hartmann, T. of Lupin Alkaloids. Researchgate.

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6. Seiple, B. (2006) The Lupin Alkaloids. Baran Group Meeting.

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7. Reid, M. B. (1998). Role of nitric oxide in skeletal muscle: synthesis, distribution and functional importance. Acta physiologica Scandinavica,162(3), 401-409.

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8. Gunst, S. J., & Wu, M. F. (2001). Plasticity in Skeletal, Cardiac, and Smooth Muscle: Selected Contribution: Plasticity of airway smooth muscle stiffness and extensibility: role of length-adaptive mechanisms. Journal of Applied Physiology, 90(2), 741.

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9. Morse, C. I., Wüst, R. C., Jones, D. A., De Haan, A., & Degens, H. (2007). Muscle fatigue resistance during stimulated contractions is reduced in young male smokers. Acta physiologica, 191(2), 123-129.

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10. Pesta, D. H., Angadi, S. S., Burtscher, M., & Roberts, C. K. (2013). The effects of caffeine, nicotine, ethanol, and tetrahydrocannabinol on exercise performance. Nutrition & metabolism, 10(1), 1.

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11. Pabreza, L. A., Dhawan, S., & Kellar, K. J. (1991). [3H] cytisine binding to nicotinic cholinergic receptors in brain. Molecular Pharmacology, 39(1), 9-12.

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12. Pesta, D. H., Angadi, S. S., Burtscher, M., & Roberts, C. K. (2013). The effects of caffeine, nicotine, ethanol, and tetrahydrocannabinol on exercise performance. Nutrition & metabolism, 10(1), 1.

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13. Rezvani, A. H., & Levin, E. D. (2001). Cognitive effects of nicotine. Biological psychiatry, 49(3), 258-267.

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14. Winders, S. E., & Grunberg, N. E. (1990). Effects of nicotine on body weight, food consumption and body composition in male rats. Life sciences, 46(21), 1523-1530.

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15. Gurrola-Díaz, C. M., Borelli, M. I., Przybyl, A. K., García-López, J. M., Garzón-de la Mora, P., García-López, P. M., & Berger, J. D. (2008). Insulin secretion effect of 2, 17-dioxosparteine, 17-thionosparteine, multiflorine and 17-hydroxy-lupanine on rat Langerhan’s islets. In Proceedings of the 12th International Lupin Conference—Lupins for health and wealth (pp. 484-487).

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16. Abdel, H. O., Abdel, F. H., Halim, A. F., & Murakoshi, I. (1997). Comparative chemical and biological studies of the alkaloidal content of Lygos species and varieties growing in Egypt. Acta Pharmaceutica Hungarica, 67(6), 241-247.

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17. Kubo, H., Inoue, M., Kamei, J., & Higashiyama, K. (2006). Hypoglycemic effects of multiflorine derivatives in normal mice. Biological and Pharmaceutical Bulletin, 29(10), 2046-2050.

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18. Kahn, S. E., Hull, R. L., & Utzschneider, K. M. (2006). Mechanisms linking obesity to insulin resistance and type 2 diabetes. Nature, 444(7121), 840-846.

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19. Thorell, A., Hirshman, M. F., Nygren, J., Jorfeldt, L., Wojtaszewski, J. F., Dufresne, S. D., & Goodyear, L. J. (1999). Exercise and insulin cause GLUT-4 translocation in human skeletal muscle. American Journal of Physiology-Endocrinology And Metabolism, 277(4), E733-E741.

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20. Terada, S., Yokozeki, T., Kawanaka, K., Ogawa, K., Higuchi, M., Ezaki, O., & Tabata, I. (2001). Effects of high-intensity swimming training on GLUT-4 and glucose transport activity in rat skeletal muscle. Journal of Applied Physiology, 90(6), 2019-2024.

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21. Bingham, E. M., Hopkins, D., Smith, D., Pernet, A., Hallett, W., Reed, L., & Amiel, S. A. (2002). The role of insulin in human brain glucose metabolism an 18fluoro-deoxyglucose positron emission tomography study. Diabetes, 51(12), 3384-3390.

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22. Mergenthaler, P., Lindauer, U., Dienel, G. A., & Meisel, A. (2013). Sugar for the brain: the role of glucose in physiological and pathological brain function. Trends in neurosciences, 36(10), 587-597.

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23. Sugaya, K., Giacobini, E., & Chiappinelli, V. A. (1990). Nicotinic acetylcholine receptor subtypes in human frontal cortex: changes in Alzheimer's disease. Journal of neuroscience research, 27(3), 349-359.

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24. Buccafusco, J. J., Letchworth, S. R., Bencherif, M., & Lippiello, P. M. (2005). Long-lasting cognitive improvement with nicotinic receptor agonists: mechanisms of pharmacokinetic–pharmacodynamic discordance. Trends in pharmacological sciences, 26(7), 352-360.

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25. Arneric, S. P., Sullivan, J. P., Decker, M. W., Brioni, J. D., Bannon, A. W., Briggs, C. A., & Williams, M. (1995). Potential treatment of Alzheimer disease using cholinergic channel activators (ChCAs) with cognitive enhancement, anxiolytic-like, and cytoprotective properties. Alzheimer Disease & Associated Disorders, 9, 50-61.

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26. Benedict, C., Hallschmid, M., Hatke, A., Schultes, B., Fehm, H. L., Born, J., & Kern, W. (2004). Intranasal insulin improves memory in humans. Psychoneuroendocrinology, 29(10), 1326-1334.

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27. Manuel Gomez Saez, J. (2012). Possible usefulness of growth hormone/insulin-like growth factor-I axis in Alzheimer's disease treatment. Endocrine, Metabolic & Immune Disorders-Drug Targets (Formerly Current Drug Targets-Immune, Endocrine & Metabolic Disorders), 12(3), 274-286.

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28. Yakar, S., Pennisi, P., Kim, C. H., Zhao, H., Toyoshima, Y., Gavrilova, O., & LeRoith, D. (2004). Studies involving the GH-IGF axis: Lessons from IGF-I and IGF-I receptor gene targeting mouse models. Journal of endocrinological investigation, 28(5 Suppl), 19-22.

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29. Turner, J. D., Rotwein, P., Novakofski, J., & Bechtel, P. J. (1988). Induction of mRNA for IGF-I and-II during growth hormone-stimulated muscle hypertrophy. American Journal of Physiology-Endocrinology And Metabolism, 255(4), E513-E517.

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30. Emmison, N., Agius, L., & Zammit, V. A. (1991). Regulation of fatty acid metabolism and gluconeogenesis by growth hormone and insulin in sheep hepatocyte cultures. Effects of lactation and pregnancy. Biochemical journal, 274(1), 21-26.

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31. Fain, J. N., Kovacev, V. P., & Scow, R. O. (1965). Effect of growth hormone and dexamethasone on lipolysis and metabolism in isolated fat cells of the rat. Journal of Biological Chemistry, 240(9), 3522-3529.

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32. Chia, D. J., Ono, M., Woelfle, J., Schlesinger-Massart, M., Jiang, H., & Rotwein, P. (2006). Characterization of distinct Stat5b binding sites that mediate growth hormone-stimulated IGF-I gene transcription. Journal of Biological Chemistry, 281(6), 3190-3197.

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33. Gorden, P., Hendricks, C. M., Kahn, C. R., Megyesi, K., & Roth, J. (1981). Hypoglycemia associated with non-islet-cell tumor and insulin-like growth factors: a study of the tumor types. New England Journal of Medicine, 305(24), 1452-1455.

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34. Manuel Gomez Saez, J. (2012). Possible usefulness of growth hormone/insulin-like growth factor-I axis in Alzheimer's disease treatment. Endocrine, Metabolic & Immune Disorders-Drug Targets (Formerly Current Drug Targets-Immune, Endocrine & Metabolic Disorders), 12(3), 274-286.

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35. Hoshaw, B. A., Malberg, J. E., & Lucki, I. (2005). Central administration of IGF-I and BDNF leads to long-lasting antidepressant-like effects. Brain research, 1037(1), 204-208.

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36. Obermayr, R. P., Mayerhofer, L., Knechtelsdorfer, M., Mersich, N., Huber, E. R., Geyer, G., & Tragl, K. H. (2005). The age-related down-regulation of the growth hormone/insulin-like growth factor-1 axis in the elderly male is reversed considerably by donepezil, a drug for Alzheimer's disease. Experimental gerontology, 40(3), 157-163.

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37. Dobren'kov, A. G., Tilyabaev, Z., Dalimov, D. N., & Abduvakhabov, A. A. (1988). Anabasine and cytisine derivatives as reversible cholinesterase inhibitors. Chemistry of Natural Compounds, 24(1), 85-88.

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