Sayer Ji
Founder of

Subscribe to our informative Newsletter & get two FREE E-Books

Our newsletter serves 250,000 with essential news, research & healthy tips, daily.

Easy Turmeric recipes + The Dark Side of Wheat

GMO Insulin Increases Morbidity and Mortality in Type 2 Diabetics

GMO Insulin Increases Morbidity and Mortality in Type 2 Diabetics

Studies show that synthetic, genetically modified insulin could be to blame for a number of complications in diabetes patients.

Type 2 diabetes mellitus (T2DM), also known as non-insulin dependent diabetes mellitus, is reported to be one of the oldest diseases known to mankind, first documented three thousand years ago in an Egyptian manuscript (1). One of the sequelae of metabolic syndrome, type 2 diabetes is characterized by hyperglycemia and insulin resistance, which manifests as relative insulin deficiency (2). Insulin, generated by the pancreas, is the hormonal signal produced with sugar or carbohydrate consumption, that enables influx of glucose into the cells to fuel energy-demanding processes. Thus, the insulin resistance which is the cardinal attribute of type 2 diabetes leads to impaired glucose transport to muscle, liver, and adipose cells (2).

In comparison, type 1 diabetes, which is delineated insulin-dependent diabetes mellitus, arises secondary to insulin deficiency as a result of autoimmune-mediated destruction of the insulin-producing beta cells of the pancreas (3). Compared to type 2 diabetes, type 1 diabetes may necessitate immediate need for exogenous insulin replacement (4). However, with type 2 diabetes, insulin insensitivity leads to declining insulin production and ultimately pancreatic beta-cell failure (2).

The constellation of risk factors that denote metabolic syndrome, including visceral adiposity, hypertension, and hyperlipidemia, are well-elucidated to augment risk for type 2 diabetes (5). Obesity, for example, a hallmark of metabolic syndrome, contributes to just over half of cases of type 2 diabetes (2). Ectopic fat deposition, or the accumulation of triglycerides in liver, muscle, and pancreatic cells, is also implicated in the pathophysiology of type 2 diabetes, alongside mitochondrial dysfunction and derangements in adipokine synthesis by fat tissue (6, 7).

Although it is classically considered a disease of affluence, eighty percent of people with diabetes mellitus live in low- and middle-income countries (2). In the United States, 25.8 million people were afflicted by diabetes mellitus in 2010, with the vast majority having type 2 diabetes (8). Worldwide, however, 415 million people suffer from diabetes mellitus, and projections estimate that 642 million will be afflicted by 2030 (9). Due to the toll diabetes incurs upon quality of life as well as the cost to the health care system resulting from long-term sequelae of diabetes, including microvascular complications such as nephropathy, retinopathy, and neuropathy as well as occult macrovascular disease and atherosclerosis, prevention-oriented approaches should be first line strategies to combating the diabetes epidemic (10).

Elevated Plasma Glucose Mediates Diabetic Complications

Pharmacotherapy including biguanides, sulfonylureas, meglitinides, alpha-glucosidase inhibitors, incretin-based therapies, bromocriptine, dipeptidyl-peptidase IV inhibitors and thiazolidinediones, each with their attendant risks, are all employed to treat type 2 diabetes within the conventional biomedical paradigm (2). In some cases, insulin replacement is employed as a hypoglycemic agent to mitigate the glucotoxicity, or elevated blood glucose, that accompanies diabetes.

Endogenous insulin lowers blood glucose by recruiting glucose transporter isoform GLUT4 to the plasma membrane of the cell (11). Insulin has been demonstrated to both increase the intrinsic activity of this facilitative GLUT4 transporter, as well as induce translocation of GLUT4 transporters from intracellular pools to the cell surface (11).

Withdrawal of circulating glucose is important because chronic hyperglycemia mediates the complications of diabetes, including retinopathy, nephropathy, and neuropathy (11). In addition to vascular endothelial cells, pancreatic β cells are particularly vulnerable to elevated plasma glucose, which perpetuates the cycle of hyperglycemia such that “ensuing β-cell dysfunction promotes decreased insulin synthesis and secretion” (11, p. 90). Thus, glycemic control is a paramount objective in diabetes care.

The Dark Side of Insulin: Death and Debility

Although early insulization is recommended as standard of care by the American Diabetes Association and European Association for the Study of Diabetes, “the risk–benefit profile of exogenous insulin in the management of people with T2DM has also undergone scrutiny” (12). A Canadian study by Gamble and colleagues (2010), for example, revealed a graded relationship between insulin exposure and mortality. A 1.75-fold, 2.18-fold, and 2.79-fold increased risk of death was discovered for those with low, moderate, and high levels of insulin exposure, respectively, compared to controls (13).

Similarly, a retrospective analysis following 6484 subjects for 3.3 years illuminated that “There was an association between increasing exogenous insulin dose and increased risk of all-cause mortality, cancer and MACE [major adverse cardiovascular events] in people with type 2 diabetes” (14). Every one unit increase in insulin dose administered to type 2 diabetics enhanced risk of all-cause mortality by 54%, increased risk of major adverse cardiovascular events by 37%, and increased risk of cancer by 35% (14). Another retrospective cohort study in the United Kingdom illuminated that insulin treatment in type 2 diabetics increased mortality by 50% compared to metformin plus sulfonylurea (15).

Likewise, in a study of 84,622 type 2 diabetes patients, insulin monotherapy increased risk of major adverse cardiac events by 73.6%, myocardial infarction by 95.4%, stroke by 43.2%, cancer by 43.7%, and eye complications by 17.1% (12). Insulin administration also increased neuropathy by 2.146-fold, renal complications by 3.504-fold, and all cause mortality by 2.197-fold (12). The authors underscore that, “When compared directly, aHRs [adjusted hazard ratios] were higher for insulin monotherapy vs all other regimens for the primary end point and all-cause mortality” (12).

Insulin Treatment Worsens Cardiovascular Outcomes

This same trend is confirmed by another study demonstrating that insulin treatment in diabetic patients with advanced heart failure is correlated with a significantly worse prognosis, so much so that even after adjustment for extraneous variables such as duration of diabetes, “ insulin-treated diabetes was found to be an independent predictor of mortality” (16, p. 168). In fact, survival rate at one year was 85.8% for non-insulin-treated diabetic patients versus 62.1% for insulin-treated diabetic patients, illustrating the dramatic disparity in outcomes (16). The hazard ratio (HR) for insulin-treated diabetes at one and two years was 4.30 and 4.96, respectively, indicating a four- to five-fold increased rate of mortality with insulin treatment (16).

Similarly, insulin treatment worsened recovery in type 2 diabetics with congestive heart failure (CHF) who underwent cardiac resynchronization therapy (CRT), a treatment aimed at improving cardiovascular performance and survival in CHF (17). Whereas the death rate was 8.63 per 100 patients-year in non insulin-treated diabetics, it was 15.84 in the insulin-treated diabetic cohort (17).

Along the same lines, a large study of post-myocardial infarction (MI) patients highlighted that insulin treatment dramatically increased risk of mortality in diabetic patients compared to those treated with diet and other medications and MI patients without diabetes (18).

Association Between Insulin and Cancer

Studies have indicated that diabetic patients exposed to insulin incur higher rates of cancer risk and mortality. According to researchers, “We also observed a strong gradient of cumulative insulin dispensations and cancer mortality rates in this population. Compared with patients not exposed to insulin therapy, we observed a significantly increased risk of death from cancer associated with increases in cumulative exogenous insulin exposure” (19).

One hospital-based case-control study revealed that “diabetic patients who had taken insulin or insulin secretagogues had a significantly higher risk of pancreatic cancer compared with diabetic patients who had not taken these drugs” (20). Other studies have proven a link between insulin therapy and significantly increased rates of colorectal cancer in type 2 diabetics compared to non-insulin users (21). Specifically, after adjusting for potential confounding variables, each incremental year of insulin therapy was associated with a 21% increased risk of colorectal cancer (21). These results were replicated by Chung and colleagues, who found a three-fold elevated risk for colorectal adenoma in type 2 diabetic patients who received chronic insulin therapy relative to those who received no insulin (22).

How Insulin Engenders Morbidity and Mortality: Mechanisms of Action

Because interventional studies are scarce, much of the scientific data on this subject matter is derived from epidemiological studies. The argument that correlation cannot be conflated with causation has merit; however, the preponderance of literature indicates that insulin use is associated with substantial risks that warrant further investigation.

Although it is possible that insulin use may represent a surrogate marker for more advanced disease, many studies such as the analysis by Smooke and colleagues (2005) have adjusted for this confounding factor (16). Risk of mortality conferred by insulin use remained after accounting for different baseline characteristics, including age, sex, body mass index, serum creatinine, history of coronary artery disease or hypertension, and ejection fraction (16).

Another possibility researchers propose is that patients on insulin monotherapy are missing out on benefits conferred by oral anti-diabetic medications, or that they failed these medications due to poor compliance (16). More tenable is the possibility that insulin augments cardiovascular risk because “Insulin has been associated with increased sympathetic nervous system activation, increased vascular resistance, increased cardiac and vascular hypertrophy, and endothelial dysfunction” (16). In this way, insulin, which also has demonstrated atherogenic properties, may contribute to the development and progression of heart failure (19).

Additionally, as a growth hormone, insulin possesses mitogenic properties, meaning that it encourages cell division in a way that could contribute to cancer development (19). In concert with elevated levels of IGF-1, hyperinsulinemia may promote the proliferation of neoplastic cell lines (23). Thus, insulin administration may exacerbate pre-existing hyperinsulinemia in patients with type 2 diabetes, leading to accelerated cancer development (19).

Type 2 Diabetics Insulin Use May Culminate in Double Diabetes

In one Japanese study, insulin administration led to rapid deterioration of glucose control, decline in C-peptide to levels reflective of insulin deficiency, and onset of type 1 diabetes after a mean duration of 7.7 ± 6.1 months (24). Further, islet cell related autoantibodies indicative of type 1 diabetes became positive in three cases (24). In type 1 diabetes, it is speculated that genetic susceptibility is primarily conferred by presence of human leukocyte antigen (HLA) class II region (IDDM1) and the insulin gene region (IDDM2), both of which were present in this cohort (25).

Insulin administration has previously been reported in the literature to incite type 1 diabetes in three genetically predisposed type 2 diabetic patients as well (26). Insulin therapy led to various immunological responses, including insulin antibody production, insulin allergy, and infiltration of mononuclear cells in to pancreatic islets (26). Insulin is the predominant β-cell auto-antigen implicated in the pathophysiology of type 1 diabetes, and auto-reactivity of CD4+ and CD8+ T cells to insulin epitopes has been demonstrated in type 1 diabetics (27, 28). Thus, researchers conclude that “insulin may play an essential role in the pathogenesis of T1DM [type 1 diabetes mellitus]” (24).

Is Genetically Modified Insulin to Blame?

This double diabetes, or development of autoimmune insulin-deficient type 1 diabetes following treatment of insulin-resistant type 2 diabetes, as well as the host of other adverse sequelae associated with insulin use in type 2 diabetics, may be due in part to the genetic recombinant insulin preparations that are the brainchild of the biotech industry.

As previously reported, the three-dimensional conformation of synthetic, genetically modified (GM) insulin diverges dramatically from the porcine-derived insulin that it displaced from the market. Because structure dictates function, even point amino acid substitutions, which are routinely utilized in the development of insulin analogs, can result in different ionic interactions, hydrogen bonding, hydrophobic packing, and Van der Waals forces between amino acids in proteins that in turn give rise to markedly different spatial folding patterns (29).

There is, for example, a disparity in primary structure between bioidentical insulin and one of the best-selling insulin analog Lantus (insulin glargine [rDNA origin] injection). Produced from a genetically engineered strain of Escherichia coli (E. coli), “Insulin glargine differs from human insulin in that the amino acid asparagine at position A21 is replaced by glycine and two arginines are added to the C-terminus of the B-chain” (30). Changes in primary structure, or sequence of amino acid residues, are translated into changes in geometric secondary structure, interactions between motifs known as super secondary structure, and interactions among protein domains, such as disulfide bonding, known as tertiary structure. Due to the principal that structure governs function, these modifications can result in deleterious functional changes.

GMO Insulin Cannot Replicate the Physiological Activity of Native Insulin

Because insulin is a water-soluble hormone, it cannot freely penetrate the lipid bilayer and diffuse into the cell to elicit biological effects (31). For native insulin to bind to its proper receptors and exert its life-sustaining effects, it must be folded, for instance, into spiral alpha-helices and beta-pleated sheets, laterally packed adjacent to parallel or antiparallel beta strands (31).

Compared with endogenous insulin, manmade GM acylated long-acting insulins may exhibit reduced metabolic activity, as the addition of a fatty acid chain alters its binding affinity for its cognate receptor and even distorts its self-assembly capacity (32, 33). Due to the reduced potency of these formulations, such as detemir, they are designed to be administered at fourfold higher concentrations relative to other insulin analogs (31).

Scientists have also speculated that misfolding of manmade GM insulin can create insulin cross-linking with proteins in endothelial cells, plasma membranes, and vascular walls (34). For instance, changes in protein conformation due to misfolding of acetylated recombinant insulins such as detemir and degludec may cause binding of insulin preparations to albumin, the primary protein in human blood plasma, which results in higher circulating levels of these insulin products (31). Structural and allosteric modifications to degludec have resulted in its ability to create multi-hexamers deposited in subcutaneous tissue (35).

With regard to these synthetic insulin products, Monnier and colleagues (2014) echo these sentiments, with,

“All chemical modifications of the insulin molecule, including elongation with two arginine residues at the C terminus of the B-chain (insulin glargine), and acylation of the hormone with a fatty acid either directly (insulin detemir) or indirectly (insulin degludec) added to the B-chain, can alter the effects of these long-acting insulin analogues on such parameters as glucose transport to cells, stimulation of multiple intracellular pathways and activation of mitogenic processes” (31).

Lastly, if it assumes an inappropriate folding pattern, it is possible that synthetic, GM insulin is recognized as a foreign entity, which may results in immunogenic reactions (31). Because it is unable to assume the native protein structure, GM insulin may not only be unable to perform the life-sustaining functions of endogenous insulin, but it also has the potential to elicit maladaptive immune responses.

Natural Anti-Diabetic Substances

In many cases, insulin treatment in type 2 diabetes, a disorder of deranged insulin signaling, may represent adding fuel to the fire. No individual should misconstrue this article as medical advice or discontinue any medication without the approval of a licensed physician. The intent, rather, is to encourage early dietary and lifestyle interventions, combined with targeted nutraceuticals, in order to prevent the downward trajectory that results in the prescribing of insulin to treat type 2 diabetes.

Although there is a strong genetic component, researchers maintain that the majority of cases of type 2 diabetes can be prevented through lifestyle modifications (2). Variables, such as cigarette smoking, alcohol consumption, a sedentary lifestyle, obesity, and toxicant exposure are all preventable factors correlated with development of type 2 diabetes (36, 2).

In addition, as catalogued in the GreenMedInfo databases, dozens of natural agents and modalities, including botanicals such as ginger (37), spirulina (38), and black cumin seed (39), nutraceuticals such as L-arginine (40), vitamin C (41), magnesium (42), omega-3 fatty acids (43), and vitamin D (43), and both high intensity interval training (44) and aerobic exercise (45) have all demonstrated anti-diabetic and insulin-sensitizing effects in human trials. Consistent with naturopathic precepts, health care providers should prioritize these lowest risk, least invasive interventions as the standards of care.


1. Ahmed, A.M. (2002). History of diabetes mellitus. Saudi Medical Journal, 23(4), 373-378.

2. Olokoba, A.B. et al. (2012). Type 2 Diabetes Mellitus: A Review of Current Trends. Oman Medical Journal, 27(4), 269-273.

3. Todd, J.A. (2010). Etiology of type 1 diabetes. Immunity, 32, 457–467.

4. Atkinson, M.A., Eisenbarth, G.S., & Michels, A.W. (2014). Type 1 diabetes. Lancet, 383(9911), 69-82.

5. Alberti, K.G. et al. (2005). The metabolic syndrome—a new worldwide definition. Lancet, 366(9491), 1059-1062. doi: 10.1016/S0140-6736(05)67402-8

6. Garcia-Roves, P.M. (2011). Mitochondrial pathophysiology and type 2 diabetes mellitus. Archives of Physiology and Biochemistry, 117(3), 177-187.

7. Fujioka, K. (2007). Pathophysiology of type 2 diabetes and the role of incretin hormones and beta-cell dysfunction. Journal of the American Academy of Physicians, Suppl 3-8.

8. Department of Health and Human Services. Centres for Disease Control and Prevention, (2011). National diabetes fact sheet: national estimates and general information on diabetes and prediabetes in the United States, 2011. Retrieved from

9. Global Burden of Diabetes. (2011). International Diabetes Federation. Diabetic Atlas SeventhEdition. Retrieved from

10. Stolar, M. (2010). Glycemic control and complications in type 2 diabetes mellitus. American Journal of Medicine, 123 (3 Suppl), S3-S11. doi: 10.1016/j.amjmed.2009.12.004.

11. Furtado, L.M. et al. (2002). Activation of the glucose transporter GLUT4 by insulin. Biochemistry and Cell Biology, 80(5), 569-578.

12. Currie, C.J. et al. (2013). Mortality and other important diabetes-related outcomes with insulin vs other antihyperglycemic therapies in type 2 diabetes. Clinical Endocrinology and Metabolism, 98(2), 668-777.  doi: 10.1210/jc.2012-3042.

13. Gamble, J.M. et al. (2010). Insulin use and increased risk of mortality in type 2 diabetes: a cohort study. Diabetes, Obesity, and Metabolism, 12(1), 47-53. doi: 10.1111/j.1463-1326.2009.01125.x.

14. Holden, S.E. et al. (2015). Glucose-lowering with exogenous insulin monotherapy in type 2 diabetes: dose association with all-cause mortality, cardiovascular events and cancer. Diabetes, Obesity, and Metabolism, 17(4), 350-362. doi: 10.1111/dom.12412.

15. Currie, C.J. et al. (2010). Survival as a function of HbA1c in people with type 2 diabetes: a retrospective cohort study. Lancet, 375, 481–489.

16. Smooke, S., Horwich, T.B., & Fonarow, G.C. (2005). Insulin-treated diabetes is associated with a marked increase in mortality in patients with advanced heart failure. American Heart Journal, 149(1), 168-174.

17. Mangiavacchi, M. et al. (2008). Insulin-treated type 2 diabetes is associated with a decreased survival in heart failure patients after cardiac resynchronization therapy. Pacing and Clinical Electrophysiology, 31(11), 1425-1432. doi: 10.1111/j.1540-8159.2008.01206.x.

18. Berger, A.K. et al. (2001). Effect of diabetes mellitus and insulin use on survival after acute myocardial infarction in the elderly (the Cooperative Cardiovascular Project). American Journal of Cardiology, 87, 272-277.

19. Bowker, S.L. et al. (2010). Glucose-lowering agents and cancer mortality rates in type 2 diabetes: assessing effects of time-varying exposure. Diabetologia, 53(8), 1631-1637.

20. Li, D. et al. (2009). Antidiabetic therapies affect risk of pancreatic cancer. Gastroenterology, 137(2), 482-488. doi: 10.1053/j.gastro.2009.04.013.

21. Yang, Y.X. et al. (2004). Insulin therapy and colorectal cancer risk among type 2 diabetes mellitus patients. Gastroenterology, 127(4), 1044-1050.

22. Chung, Y.W. et al. (2008). Insulin therapy and colorectal adenoma risk among patients with Type 2 diabetes mellitus: a case-control study in Korea. Diseases of the Colon and Rectum, 51(5), 593-597. doi: 10.1007/s10350-007-9184-1.

23. Pollak, M. (2008). Insulin and insulin-like growth factor signaling in neoplasia. Nature Reviews, 8, 915-9928.

24. Nishida, W. et al. (2014). Insulin administration may trigger type 1 diabetes in Japanese type 2 diabetes patients with type 1 diabetes high-risk HLA class II and the insulin gene VNTR genotype. Journal of clinical Endocrinology and Metabolism, 99(9), E1793-E1797. doi: 10.1210/jc.2014-1759.

25. Ounissi-Benkalha, H., & Polychronakos, C. (2008). The molecular genetics of type 1 diabetes: new genes and emerging mechanisms. Trends in Molecular Medicine, 14(6), 268-275. doi: 10.1016/j.molmed.2008.04.002.

26. Nakamura, M. et al. (2008). Insulin administration may trigger pancreatic β-cell destruction in patients with type 2 diabetes. Diabetes Research in Clinical Practice, 79, 220-229.

27. Di Lorenzo, T.P., Peakman, M., & Roep, B.O. (2007). Translational mini-review series on type 1 diabetes: Systematic analysis of T cell epitopes in autoimmune diabetes. Clinical Experiments in Immunology, 148(1), 1-16.

28. Nagata, M. et al. (2007). Immunological aspects of “fulminant type 1 diabetes.” Diabetes Research and Clinical Practice, 77S, S99–S103.

29. Žáková, L. et al. (2014). Human insulin analogues modified at the B26 site reveal a hormone conformation that is undetected in the receptor complex. Acta Crystallographica Section D-Biological Crystallography Journal, 70(Pt 10), 2765-2774.

30. RxList. (2017). Lantus. Retrieved from

31. Monnier, L., Colette, C., & Owens, D. (2014). Acylated-based long-acting insulin analogues: Is “misfolding” the problem? Commentary letter on Hamasaki H and Yanai H. The switching from insulin glargine to insulin degludec reduced HbA1c, daily insulin doses and anti-insulin antibody in anti-insulin antibody-positive subjects with type 1 diabetes. Diabetes & Metabolism, 40(6), 483-484.

32. Menting, J.G. et al. (2013). How insulin engages its primary binding site on the insulin receptor, 493, 241-245.

33. Owens, D.R., Matfin, G., & Monnier, L. (2014). Basal insulin analogs in the management of diabetes mellitus: what progress have we made? Diabetes/Metabolism Research and Reviews, 30, 104-119.

34. Monnier, L., Colette, C., & Owens, D. (2013). Basal insulin analogs: from pathophysiology to therapy. What we see, know and try to comprehend. Diabetes & Metabolism, 39, 468-476.

35. Sreengard, D.B. et al. (2013). Ligand-controlled assembly of hexamers, dihexamers and linear multihexamers by the engineered acylated insulin degludec. Biochemistry, 52, 295-309.

36. Hu, F.B. et al. (2001). Diet, lifestyle, and the risk of type 2 diabetes mellitus in women. New England Journal of Medicine, 345(11), 790-797.

37. Shidfar, F. et al. (2015). The effect of ginger (Zingiber officinale) on glycemic markers in patients with type 2 diabetes. Journal of Complementary and Integrative Medicine, 12(2), 165-170. doi: 10.1515/jcim-2014-0021.

38. Marcel, A.K. et al. (2011). The effect of Spirulina platensis versus soybean on insulin resistance in HIV-infected patients: a randomized pilot study. Nutrients, 3(7), 712-724. doi: 10.3390/nu3070712.

39. Bamosa, A.O. et al. (2010). Effect of Nigella sativa seeds on the glycemic control of patients with type 2 diabetes mellitus. Indian Journal of Physiology and Pharmacology, 54(4), 344-354.

40. Piatti, P.M. (2001). Long-term oral L-arginine administration improves peripheral and hepatic insulin sensitivity in type 2 diabetic patients. Diabetes Care, 24(5), 875-880.

41. Mason, S.A. (2016). Ascorbic acid supplementation improves skeletal muscle oxidative stress and insulin sensitivity in people with type 2 diabetes: Findings of a randomized controlled study. Free Radical Biology Medicine, 93, 227-238. doi: 10.1016/j.freeradbiomed.2016.01.006.

42. Moctezuma-Velázquez, C. (2017). High Dietary Magnesium Intake is Significantly and Independently Associated with Higher Insulin Sensitivity in a Mexican-Mestizo Population: A Brief Cross-Sectional Report. Revista De Investigacion Clinica, 69(1), 40-46.

43. Jamilian, M. et al. (2017). The effects of vitamin D and omega-3 fatty acid co-supplementation on glycemic control and lipid concentrations in patients with gestational diabetes. Journal of Clinical Lipidology, 11(2), 459-468. doi: 10.1016/j.jacl.2017.01.011.

44. Jelleyman, C. et al. (2015). The effects of high-intensity interval training on glucose regulation and insulin resistance: a meta-analysis. Obesity Reviews, 16(11), 942-961. doi: 10.1111/obr.12317.

45. van der Heijden, G.J. (2010). A 12-week aerobic exercise program reduces hepatic fat accumulation and insulin resistance in obese, Hispanic adolescents. Obesity (Silver Spring), 18(2), 384-390. doi: 10.1038/oby.2009.274.

Disclaimer: This article is not intended to provide medical advice, diagnosis or treatment. Views expressed here do not necessarily reflect those of GreenMedInfo or its staff.
Sayer Ji
Founder of

Subscribe to our informative Newsletter & get two FREE E-Books

Our newsletter serves 250,000 with essential news, research & healthy tips, daily.

Easy Turmeric recipes + The Dark Side of Wheat

This website is for information purposes only. By providing the information contained herein we are not diagnosing, treating, curing, mitigating, or preventing any type of disease or medical condition. Before beginning any type of natural, integrative or conventional treatment regimen, it is advisable to seek the advice of a licensed healthcare professional.

© Copyright 2008-2017, Journal Articles copyright of original owners, MeSH copyright NLM.