Support for people with diabetes, pre-diabetes & those at risk for diabetes.
20 years of scientific studies that prove the benefits of Lysulin’s ingredients
Lysine Lowers Glucose and Glycated Proteins
Am J Clin Nutr. 2009 90 (2):314-20. “Lysine ingestion markedly attenuates the glucose response to ingested glucose without a change in insulin response”.
Diab/Metab Res Rev 2008 24: 64-73 – Four month study with diabetic rats. Lysine inhibits protein glycation and lowers blood glucose.
Acta medica Iranica 54 January 2016 24-31. “The findings…provide convincing evidence on the usefulness of lysine supplementation as a new adjunct therapy for diabetes.
Diabetologia (1993) 36: 797-801- Diabetic rat study. this study has demonstrated that lysine treatment in chemically-induced diabetes is capable of reducing glycated proteins and it could potentially delay the appearance of the late pathologies associated with diabetic hyperglycemia and aging.
Alternative Medicine Review 2007, 12, # 2, 169-172. Reports amazing utility of lysine for treatment of herpes. “In general, lysine supplementation is very safe. Doses up to 3 g daily are typically well-tolerated.”
Med Sci Monit, 2002 8(3) 131-137. In study with 77 Type 2 patients divided into 4 groups. HbA1c dropped from 9 to 8.2% in group taking lysine.
Exp. Eye Res. (1998) 67, 597-601. While the blood sugar levels remain high in the diabetic controls, there was a phenomenal reduction of blood sugar levels in lysine or amino acids-fed groups. Lysine in particular has the prospect of therapeutic value in the control of diabetes. Normal levels of glycosylated hemoglobin in groups III and IV confirm diabetic control by lysine. The mechanism may be mostly through scavenging of glucose by amino acids. All the diabetic rats developed cataract (Fig. 1) at the end of 70-90 days. Interestingly, four out of six in group IV receiving lysine alone or amino acids orally did not develop cataract. Dietary intake a mixture of essential amino acids, chiefly lysine, may ward off or delay cataract formation.
Complementary and Alternative Medicine (2015) 15:193, It was concluded that, lysine attenuates pancreatic tissue injury induced by L-arginine by inhibiting the release of the inflammatory cytokine as IL-6 and enhance antioxidant capacity.
Eye Res 1993 56, 623-628. Lysine and glucose undergo non-enzymatic glycation ay physiological pH and temperature with glucose and compete for this reaction with lens proteins. Lysine lowered the extent of glycation of lens proteins significantly in glucose-treated homogenates of normal lens from humans. Scavenging of intracellular glucose and thereby protecting the lens proteins from excessive glycation appears to be the mechanism of action by which lysine could exercise a beneficial effect on cataract formation.
Diabetes/metabolism research and reviews 2008 24 (1) 64-73. “RESULTS: We found that L-Lysine therapy prevented diabetic- induced increases in Glucose, AGE, HbA(1c), triglyceride, total- and LDL- cholesterol.”
Zinc Lowers Glucose and Glycated Proteins and Improves the Lipid Profile.
J Diabetes 2017 http://dx.doi.org/10.1111/1753-0407.12621. “Zinc supplementation reduced blood glucose and insulin resistance, while improving β-cell function. Furthermore, disease progression to diabetes was reduced and beneficial effects of supplementation were also noted on total and LDL cholesterol.”
Diabetol Metab Syndr. 2012; 4: 13. Zinc Review article. “The pooled mean difference in fasting blood glucose between Zinc supplemented and placebo groups was 18.13mg/dl (95%CI:33.85,2.41; p<0.05). 2-h post-prandial blood sugar also shows a similar distinct reduction in (34.87mg/dl [95%CI:75.44; 5.69]) the Zinc treated group. The reduction in HbA1c was 0.54% (95%CI:0.86;0.21) in the Zinc treated group. There were 8 studies comparing the effects of Zinc supplementation on lipid parameters in patients with type-2 diabetes. The pooled mean difference for total cholesterol between Zinc supplemented and placebo groups was 32.37mg/dl (95%CI:57.39,7.35; p<0.05). Low-density lipoprotein cholesterol also showed a similar distinct reduction in the Zinc treated group, the pooled mean difference from random effects analysis was 11.19mg/dl (95%CI:21.14,1.25; p<0.05). Studies have also shown a significant reduction in systolic and diastolic blood pressures after Zinc supplementation “
Health, 2016, 8, 344-352. “In summary, lower zinc levels are related to end stage renal disease patients in hemodialysis and supplementation seems to be a promising approach in such cases.
Nihon Rinsho 2016 74(7):1138-43. “In this article, we describe zinc deficiency in patients with CKD. The ability that zinc supplementation improves their anemia in CKD patients is also described.”
Ren Fail 2011; 33: 466-467. “Zinc deficiency has been documented in patients with CKD. In a recent editorial, the authors reported zinc deficiency in 40%-78% of hemodialysis (HD) patients.”
Journalof Diabetes (2017) doi: 10.1111/jdb.12621. Usage of Zinc in pre-diabetes: A clinical trial. 200 patients with prediabetes studied in a double-blind study. “The FPG, OGTT, total and LDL cholesterol were significantly reduced in the Zinc group, with significant improvement in β-cell function.” LDL dropped by 28% and beta cell function improved by 57%. In a 2 year follow up, fewer patients on zinc went on to develop Type 2 diabetes; 11% on zinc versus 25% in control group.
Diabetology & Metabolic Syndrome (2012), 4:13. “In conclusion, this first comprehensive systematic review and meta-analysis on the effects of Zinc supplementation in patients with diabetes demonstrates that Zinc supplementation has beneficial effects on glycemic control and promotes healthy lipid parameters.
Nutrition & Metabolism (2015) 12:26. Zinc supplementation significantly reduced total cholesterol, LDL cholesterol and triglycerides. In addition to that, Zinc supplementation in non-healthy patients demonstrated a significant elevation of HDL cholesterol. Therefore it may have the potential to reduce the incidence of atherosclerosis related morbidity and mortality especially in non-healthy patients who are at risk of atherosclerosis
DARU Journal of Pharmaceutical Sciences (2015) 23:44. “Numerous in-vitro and in-vivo studies have shown that Zinc has beneficial effects in both type-1 and type-2 diabetes. It is evident from the findings of the present systematic review, that Zinc plays an important role in β-cell function, insulin action, glucose homeostasis and the pathogenesis of diabetes and its complications.
Vitamin C Lowers Glucose and HbA1c
Advances in Pharmacological Sciences Volume (2011), Article ID 195271, doi:10.1155/2011/195271 “The absence of any substantial side effects, cheaper cost, improvement in FBS, PPBS, and HBA1c, and the fact that plasma ascorbic acid levels are decreased in DM and increased after oral supplementation make it a particularly attractive therapeutic adjuvant in the treatment of type 2 DM.
World Journal of Analytical Chemistry 2015 (1A) 6 Effect of Vitamin C on Blood Glucose and Glycosylated Hemoglobin in Type II Diabetes Mellitus. In conclusion, oral supplementation of vitamin C reduces FBG, two hours PPBG, and improves HbA1c
Glycated Proteins are the Cause of Many Disease Complications.
J Amer Col Cardiology (2017) 70: 16 2020-2021. “Glycation of HDL leads to dysfunctional HDL promoting senescence and atherosclerosis.
Dermato-Endocrinology (2012) 4:3, 259–270. “There is ample evidence that glycated proteins play an important role in skin aging.
Scars, Burns and Healing DOI: 10.1177/2059513116676828. “Abundant evidence supports the pathological effects of glycated proteins in ageing and wound healing”
Kerala Journal of Ophthalmology 2006 XVIII 3 167-173. “To sum up, protein glycation may play a pathogenic role in diabetic and age related dysfunction of the eye. The role of glycated protein in cataract formation has been extensively studied in both aged & diabetic lens where glycated proteins are significantly elevated. Glycated proteins are important in the development of age related macular degeneration. Glycated proteins are significantly increased in diabetic retinopathy patients.
Diabetes Research and Clinical Practice 67 (2005) 3–21. “Increased glycation and, in particular, accumulation of tissue and serum glycated proteins have an important role in the pathogenesis of diabetic complications. The role of glycated proteins in the pathogenesis of retinopathy, cataract, atherosclerosis, neuropathy, nephropathy, diabetic embryopathy (newborn complications with a diabetic mother) and impaired wound healing are considered.
N Engl J Med 2010 9800-811. “In nondiabetic adults, glycated hemoglobin was more strongly associated wi th risks of cardiovascular disease and death from any cause as compared with fasting glucose.”
Clinical Science (2017) 131 1069–1092. “Strong links between glycated proteins and Chronic Kidney Disease have been reported over the last 25 years.”
CURRENT SCIENCE 2002 83: 12, 1515-1521. The findings of the UKPDS which indicate for every 1% increase in glycated hemoglobin levels, a 37% increase in microvascular disease was seen.
Korean J Physiol Pharmacol 2014, 18 1-14. “Protein glycation and formation of advanced glycation end products (AGEs) play an important role in the pathogenesis of diabetic complications like retinopathy, nephropathy, neuropathy, cardiomyopathy along with some other diseases such as rheumatoid arthritis, osteoporosis and aging. Glycation of proteins interferes with their normal functions by disrupting molecular conformation, altering enzymatic activity, and interfering with receptor functioning.”
Diabetes Care 2017 40, 591-598. “In summary, these findings suggest that the effect of hyperglycemia and subsequent increased levels of AGEs in patients with long-standing Type 2 diabetes may have long-lasting adverse effects on the development of macrovascular complications.”
Neurobiology of Aging (2009) doi:10.1016/j.neurobiolaging.2009.04.016 The ‘glycation theory of aging’, as the underlying common principle of degeneration, unites some of the neuropathological and biochemical findings in Alzheimer’s Disease. AGEs may contribute to several processes underlying dementia…
SLEEP 2006; 29 (3):329-333. The formation and accumulation of advanced glycation endproducts (AGEs) has been implicated in the progression of age-related diseases such as diabetes mellitus and atherosclerosis. We hypothesize that AGE concentrations may be increased in subjects with obstructive sleep apnea (OSA). Serum levels of AGEs were increased in nondiabetic subjects with OSA and were associated with the severity of OSA.
Natl. Acad. Sci. 1995 92 3744-3748, We conclude that AGEs may contribute to the increased severity of stroke associated with diabetes and other conditions characterized by AGE accumulation.