Understanding Homeopathic Susceptibility Using a Scientific Model of Disease Origin in Type 1 Diabetes

The idea of homeopathic susceptibility is nothing more than the application of the scientific understanding of the origin of disease- Type 1 Diabetes.  By: Alia Donato, HOM, DCHM, Bsc CCHM Alumnus 2020


Am (2002) describes the etymology of diabetes which in Greek means increased urine output,  and Mellitus in Latin is defined as honey referring to urine’s sugar content. Type 1 diabetes  (T1D) is a chronic autoimmune disease and is a heterogeneous ailment identified by the  destruction of pancreatic beta cells, culminating in absolute insulin deficiency. The majority of  T1D cases are attributable to autoimmune-mediated destruction of beta cells (type 1a) while a  small minority of cases result from idiopathic destruction or failure of beta cells (type 1b)  (Michels and Gottlieb 2000). Maahs(2010) says statistically, on a worldwide scale, TID measures  up 5-10% of diabetes cases. The epidemiological patterns of this autoimmune disease are  increasing both in incidence and prevalence globally with overall annual increases in the  incidence of about 2-3% per year (Green 1992 ; Karvonen 1997) according to US data from 2001  to 2015 concluded that about 22.9 cases per 100 000 were younger than 65 years showing similar  incidences from other data regions making incidence of type 1 diabetes prominent among  children younger than 15, particularly in children younger than 5 years (Gale and Gillespie 2001;  Forga Llenas 2015).  

The causes of TID are unknown, though several risk factors have been identified, according to  Mayo Clinic (2020) some of these risk factors include:  

1. Family history, anyone with a close family member like a parent or a sibling may have a  slightly increased chance of developing diabetes,  

2. Genetics the presence of certain genes.

3. Environment exposures.  

4. Nutritional factors and their interactions. According to different fundamental and clinical  research they have suspected that these circumstances and vulnerabilities are the leading  causes for the individual who may be susceptible to T1D.  

Furthermore, to gain more insight into how these diseases come about, more research is now  being conducted to study mechanisms of susceptibility, molecular epidemiology, and functional  genomics that helps to understand and identify genes involved in individual susceptibility  (Mohammad Panah n.d.). Susceptibility is when a person may be liable to certain things within  their environment. It also investigates the vulnerability or sensitivity of an individual and how  their defensive mechanism in the human body may work. In other words, it is the state of being  predisposed and/or sensitive thereby lacking the ability to resist a specific pathogen, familial  disease, or a drug. Often when there is susceptibility, the individual may easily be harmed or  affected by things that he/she may be overly sensitive to. The way the human organism receives  or reacts to stimuli is determined by susceptibility which is important and fundamental to one's  health.

This paper will review the two sides of medicine using Homeopathy by understanding  susceptibility in the disease and conventional science in analyzing Type 1 diabetes susceptibility.  Comparing and referring to studies that include viewpoints and statements on disease  susceptibility in Homeopathy and T1D.  


Homeopathy and genetic susceptibility in TID  


Considering genetic disease susceptibility, it is understood to have a role in chromosomal and  metabolic disorders displaying often in most medical conditions. Anon (2020) states that genetics  is a structural production of proteins and enzymes where it occurs through transcription,  processing, and translation. The basis of that variation is mutation or change in the DNA  sequence, mutation occurs in every cell and when they occur in monogenic (single-gene)  diseases like diabetes can occur. These are seen in certain variants of the human leukocyte  antigen (HLA) complex genes when these genes are combined, they are called a haplotype.  Certain HLA haplotypes are correlated with developing risk of TID increasing an inappropriate  immune response to beta cells. Certain variations of mutations are silent or benign stating that  the variation in the severity of a genetic disease (polymorphisms), whereas others produce  profound consequences.  

Dr. Hahnemann the founder of homeopathy established the Homeopathic art of science medicine  in the late 1800s and mentions in his Organon in aphorism 78- the true natural chronic diseases  are from the rise of chronic miasms and is a hereditary susceptibility, it is invisible and a dynamic  disease-producing potential (Kaur 2020)- it is termed as prima causa Morbi that causes all natural disease. And if left unchecked may increase in pain or growth of the ailment which will  leave the individual suffering in pain & aggravation, during the duration of his/her lifetime. Just  like genetic susceptibility, a miasm will create obstacles in the curing process because of its  defense mechanism at a genetic level. The three underlying miasms of chronic diseases are  Psora, sychotic and Syphilis, these miasms carry their characteristics of symptoms and can often  appear together or separately in diseases. In T1D there is a combination of all the three miasms  reflecting a syphilitic miasm where there is auto-immune destruction of the b-cells, and lack of  insulin resulting in I.D.D.M(T1D), psora leading to functional disturbance resulting diminished  effectiveness leading to N.I.D.D.M(Type 2 diabetes) and sycosis due to its endocrine disharmony  and dysfunctional feedback metabolism (R. Rughani 2016).  

Environmental disease influences T1D  

Many years ago, Dr. Samuel Hahnemann pointed out that there are two basic factors for an  individual to become sick and they are an individual susceptibility and the exposure to natural  diseases and their present stressors. He then began separating true chronic disease that was  caused by mechanical or exterior conditions (aphorism 77). Dr.Herbert A (1868-1940) In The  Principals and Art of Cure by Homeopathy he found that connecting the principles of  homeopathic healing and principles and laws that govern life where he defined susceptibility as a  reaction of protective immunity against environmental conditions. He gave a sample of how  certain humans/animals even though are related may react differently in their external/internal  defence system based on the geographical conditions e.g., one individual's perniosis (skin  abnormality) may improve by the seashore while the other may fall ill, this also applies to colder  and hotter climates, as well as the person's nutrition and their inability and ability to digest certain  foods is reflected in the internal and external susceptibility (A. Roberts 2003).   


Presently, in conventional scientific research, non-genetic factors are being shown favourably in  the development of T1D placing value in environmental causation and host-related factors. An  example of this determination is on the study of monozygotic twins which indicates that 13-33%  are pairwise concordant for T1D (Barnett 1981; Kaprio 1992), meaning that during post  conception there may have been a collection of genetic discordance or exposure to different  putative exogenous material. Like this concept- Vithoulkas 1932 in his book The Science of  Homeopathy, stated miasmatic susceptibility is not just DNA or genetic composition, the  influence disease parent may transmit to their child as early as conception due to its weakened  and ill vital force which can affect the child's electrodynamic field thereby weakening its  immunity. Another scientific study example that the environment influences T1D conditions is  that Finland has an increase of T1D of 5.4-fold from the early 1950s indicating that a high  increase cannot be due to genetic disease susceptibility but mostly in the improper changes in  lifestyle and environmental conditions (Knip and Simell 2012). Including that the evidence  accumulated states that a percentage of the subjects with an elevated risk of HLA genotypes has  declined in the past decade compared to the new diagnosis of T1D. Even for individuals with low  and protected risk of HLA genotypes has increased (Hermann 2003; Rewers and Zimmet 2004)    

In this perspective both sides of medicine have acknowledged genetics and epigenetic and  environment can affect phenotype outcomes that give rise to T1D.  


Natural history of fetal and perinatal occurrences in the risk of TID  


Gluckman (2008) states Many lines of evidence, including epidemiologic data and data from  extensive clinical and experimental studies, indicate that early life events play a powerful role in  influencing later susceptibility to certain chronic diseases.  

A child's immune system starts to function already in the womb. In a 2001 article Atkinson and  Eisenbarth (2001) posits that individuals are born with various degrees of genetic susceptibility  for T1D and might occur as early as in utero and the first few months of life(Warram 1984;  Harjutsalo 2006). A mother with TID has a 2-3-fold lower risk of affecting her offspring than  TID fathers with a 7% risk (Hämäläinen and Knip 2002). Studies observed that infants of  mothers with T1D have an elevated level of regulatory T-cells in the cord blood than unaffected  TID mothers and the regulatory T-cells from infants with the affected T1D mothers are  upregulated in vitro by insulin(Luopajärvi 2012). This was also sought out by the  DIABIMMUNE study where researchers analyzed the hygiene hypothesis by investigating  infants and young children living in three close countries with a noticeable difference in the  standard of living, hygiene, TID and other immune-mediated conditions (Mustonen  2017). Stating that immunomodulation by environmental factors starts to occur during fetal life  as there was a study comparing the cord blood in children from Russian Karelia and Finnish  infants indicating these facts (Kallionpaa 2014).  


Maternal Nutrition  


Kind (2006, pg. 532-541) expressed that “Maternal nutrition influences the availability of  nutrients for transfer to the fetus”. In developing countries, a maternal lack of healthy nutrition is  a major factor in contributing to an adverse outcome, with an increased prevalence in high calorie diets resulting in overweight and obesity issues in developed countries, this impact on  over-nutrition during pregnancy is a contributing factor for adverse metabolic offspring in his/her  later life (Morrison and Regnault 2016). Though studies say that the maternal diet during  pregnancy does not bring rise to TID in the offspring (Lamb 2008; Virtanen 2010). This was  reflected in a Norwegian retrospective study, where it reported that mothers with T1D consumed  less cod liver oil during their pregnancy COD liver oil contains high concentrations of vitamin D  and omega 3 fatty acids (DHA/EPA) which are anti-inflammatory, but subsequent studies were  not able to connect an association with T1D and offspring and Omega DHA/EPA. Though supplementing with vitamin D has proven to show a decreased T1D risk. Other factor  studies analyzed that maternal smoking may reduce the risk of TID (Stene and Gale 2013)  speculating that smoking might have a modulatory effect on the immune system or DNA  methylation and that later maternal age may also affect the chance of TID (Cardwell 2009), but  the significance of these factor associations has been poor and heterogeneous concluding that the  effect is minor (Virtanen 2006).  

In homeopathy and throughout the Organon Hahnemann stated the importance of diet in various  aphorisms. Hahnemann analyzed the effect of foods and poor lifestyle like smoking is the  progression of chronic disease and the process of healing, stressing the importance of a simple,  nourishing diet and eliminating harmful habits, stating: “the careful investigation into such  obstacles to cure is so much the more necessary in the case of patients affected by chronic  diseases, as their diseases are usually aggravated by such noxious influences and other disease causing errors in the diet and regimen, which often pass unnoticed” (Organon §260) . Graves (2003) says there are also endogenous and exogenous factors as well as diseases that may  influence in the progression in T1D during conception, pre/post-pregnancy and during fetal life  and these are: congenital rubella, enterovirus infection -can boost the immune response to bovine  insulin in infants with increased HLA-defined disease predisposition high birth weight,  prematurity, older maternal age, cesarean section, early infections, CBV infections, rapid linear  growth dysbiosis, reduced microbial diversity in the gut, unregulated interferon signature before  seroconversion reduced levels of choline-containing phospholipids, changes in expression levels  of complement proteins. And early food introduction to cow's milk, cereals and certain fruits and  berries.  


Now in terms of infections and early use of endogenous/exogenous substances including  allopathic drugs. Vithoulkas (1932) explains in his book The Science of Homeopathy that based  on the principles of resonance, the organism's susceptibility to the disease-causing agents is not  only caused by virus and bacteria but emotional shocks and allopathic drugs may also cause  interference. He also states that these external influences and drug triggers can increase his/her  

susceptibility to a new variety of ailments increasing infections and virulence (Vithoulkas n.d.).  In Aphorism 73 Hahnemann says acute diseases are sporadic and rapid and affects single  individuals during various times often brought on by unhealthy and harmful influences or  exciting conditions like food poisoning, environmental temperatures; excessive cold or heat,  overuse of the body (physical strains), and emotional upsets explaining that "these diseases are  passing flare ups of a latent psora". Vithoulkas, Furthermore, discusses in detail the nature of  susceptibility which to him is mostly hereditary but can be obtained by strong infectious diseases  and current past treatments including vaccinations.  


In conclusion, the word susceptibility is the fact that an individual is liable to be affected by  external and internal influences including his/her physical environment. It is based on the  vulnerability of the individual whose constitution makes up genetics that carries a specific type  of genes that designates his/her immune system's ability to contract or fight off diseases. As well  as mentioned above genetics (family history of diseases), heritability, genetic variants, exposure  to viruses, age, obesity, nutrients, lack of exercise all have a role in T1D. The study of  epigenetics has also found links between the environment, diet and lifestyle may affect the gene  expression and lead to variant disease phenotypes like T1D.  


Hahnemann during his observation of patients noticed that patient that relapsed from chronic  treatment had patterns of diseases that were inherited by their families and that these were the  true basis of chronic diseases termed as miasms - the predisposition to acquire or inherit certain  diseases, applies also to genetic imprinting, and again can be acquired in inheritance or during  one's life. Hahnemann thought of contagious diseases as a trigger for miasms, whereas gene  imprinting can be influenced by various environmental factors. Now, conventional studies are  suggesting that environmental factors that are influential in early life have a considerable risk of  developing TID-however, there are a few environmental and host-related determinants  that have been confirmed to act as a susceptibility protector and a risk development of TID. But  the issue is that in most areas proving questionable data, is making it difficult to draw strong  conclusions in susceptibility in T1D factors(Knip 2017). So, is 'The idea of homeopathic  susceptibility nothing more than the application of the scientific understanding of the origin of  the disease? The answer is yes in most genetic and environmental predispositions the  understanding of homeopathic susceptibility in diseases is very much like the origins of Type 1  diabetes.  





 Reference list  

A. Roberts, H., 2003. Principles of homeopathy. Homeopathy, 92 (4), 232.  


Am, A., 2002. History of Diabetes Mellitus [online]. Saudi medical journal. Available from:  https://pubmed.ncbi.nlm.nih.gov/11953758/.  


Anon., 2020. Type 1 diabetes: MedlinePlus Genetics [online]. medlineplus.gov. Available from:  https://medlineplus.gov/genetics/condition/type-1-diabetes/ [Accessed 16 Feb 2021].  


Atkinson, M. A. and Eisenbarth, G. S., 2001. Type 1 diabetes: new perspectives on disease  pathogenesis and treatment. The Lancet, 358 (9277), 221–229.  


Barnett, A. H., Eff, C., Leslie, R. D. G., and Pyke, D. A., 1981. Diabetes in identical twins.  Diabetologia, 20 (2), 87–93.  


Cardwell, C. R., Stene, L. C., Joner, G., Bulsara, M. K., Cinek, O., Rosenbauer, J., Ludvigsson,  J., Jane, M., Svensson, J., Goldacre, M. J., Waldhoer, T., Jarosz-Chobot, P., Gimeno, S. G. A.,  Chuang, L.-M. ., Parslow, R. C., Wadsworth, E. J. K., Chetwynd, A., Pozzilli, P., Brigis, G., and  Urbonaite, B., 2009. Maternal Age at Birth and Childhood Type 1 Diabetes: A Pooled Analysis of  30 Observational Studies. Diabetes, 59 (2), 486–494.  


Forga Llenas, L., Goñi Iriarte, M. J., Cambra Contin, K., Ibáñez Beroiz, B., Chueca Guendulain,  M., and Berrade Zubiri, S., 2015. Incidence and temporal trends of childhood type 1 diabetes  between 1975 and 2012 in Navarre (Spain). Gaceta Sanitaria, 29 (1), 51–54.  

Gale, E. A. and Gillespie, K. M., 2001. Diabetes and gender. Diabetologia [online], 44 (1), 3–15.  Available from: https://www.ncbi.nlm.nih.gov/pubmed/11206408 [Accessed 16 Feb 2021].  


Gluckman, P. D., Hanson, M. A., Cooper, C., and Thornburg, K. L., 2008. Effect of In Utero and  Early-Life Conditions on Adult Health and Disease. New England Journal of Medicine [online],  359 (1), 61–73. Available from: https://www.nejm.org/doi/full/10.1056/NEJMra0708473.  


Graves, P. M., Rotbart, H. A., Nix, W. A., Pallansch, M. A., Erlich, H. A., Norris, J. M., Hoffman,  M., Eisenbarth, G. S., and Rewers, M., 2003. Prospective study of enteroviral infections and  development of beta-cell autoimmunity. Diabetes Research and Clinical Practice, 59 (1), 51–61.  


Green, A., Gale, E. A. M., and Patterson, C. C., 1992. Incidence of childhood-onset insulin dependent diabetes mellitus: the EURODIAB ACE study. The Lancet, 339 (8798), 905–909.  


Hämäläinen, A.-M. and Knip, M., 2002. Autoimmunity and familial risk of type 1 diabetes.  Current Diabetes Reports, 2 (4), 347–353.  


Harjutsalo, V., Reunanen, A., and Tuomilehto, J., 2006. Differential Transmission of Type 1  Diabetes from Diabetic Fathers and Mothers to Their Offspring. Diabetes, 55 (5), 1517–1524.  


Hermann, R., Knip, M., Veijola, R., Simell, O., Laine, A.-P. ., Åkerblom, H. K., Groop, P.-H. .,  Forsblom, C., Pettersson-Fernholm, K., and Ilonen, J., 2003. Temporal changes in the  frequencies of HLA genotypes in patients with Type 1 diabetes—indication of an increased  environmental pressure? Diabetologia, 46 (3), 420–425.  


Kallionpaa, H., Elo, L. L., Laajala, E., Mykkanen, J., Ricano-Ponce, I., Vaarma, M., Laajala, T.  D., Hyoty, H., Ilonen, J., Veijola, R., Simell, T., Wijmenga, C., Knip, M., Lahdesmaki, H.,  Simell, O., and Lahesmaa, R., 2014. Innate Immune Activity Is Detected Prior to Seroconversion  in Children With HLA-Conferred Type 1 Diabetes Susceptibility. Diabetes, 63 (7), 2402–2414.  


Kallionpää, H., Laajala, E., Öling, V., Härkönen, T., Tillmann, V., Dorshakova, N. V., Ilonen, J.,  Lähdesmäki, H., Knip, M., Lahesmaa, R., Koski, K., Koski, M., Ryhänen, S., Siljander, H.,  Hämäläinen, A.-M., Ormisson, A., Peet, A., Ulich, V., Kuzmicheva, E., and Mokurov, S., 2014.  Standard of hygiene and immune adaptation in newborn infants. Clinical Immunology, 155 (1),  136–147.  


Kaprio, J., Tuomilehto, J., Koskenvuo, M., Romanov, K., Reunanen, A., Eriksson, J., Stengård,  J., and Kesäniemi, Y. A., 1992. Concordance for Type 1 (insulin-dependent) and Type 2 (non insulin-dependent) diabetes mellitus in a population-based cohort of twins in Finland.  Diabetologia, 35 (11), 1060–1067.  


Karvonen, M., Pitkäniemi, M., Pitkäniemi, J., Kohtamäki, K., Tajima, N., and Tuomilehto, J.,  1997. Sex difference in the incidence of insulin-dependent diabetes mellitus: an analysis of the  recent epidemiological data. World Health Organization DIAMOND Project Group. Diabetes/


Metabolism Reviews [online], 13 (4), 275–291. Available from: https://pubmed.ncbi.nlm.nih.gov/ 9509279/ [Accessed 16 Feb 2021].  


Kaur, N., Mahajan, A., Jadhav, A., and Prof, 2020. A Clinical Study of Miasmatic Predominance  in the Management of Cases of Dysmenorrhoea in the Age Group of 15-35 Years. International  Journal of Health Sciences and Research (www.ijhsr.org) [online], 10, 4. Available from: https:// www.ijhsr.org/IJHSR_Vol.10_Issue.4_April2020/13.pdf [Accessed 16 Feb 2021].  


Kind, K. L., Moore, V. M., and Davies, M. J., 2006. Diet around conception and during  pregnancy – effects on fetal and neonatal outcomes. Reproductive BioMedicine Online, 12 (5),  532–541.  

Knip, M. and Simell, O., 2012. Environmental Triggers of Type 1 Diabetes. Cold Spring Harbor  Perspectives in Medicine [online], 2 (7). Available from: https://www.ncbi.nlm.nih.gov/pmc/ articles/PMC3385937/#A007690C30.  

  Knip, M., Luopajärvi, K., and Härkönen, T., 2017. Early life origin of type 1 diabetes. Seminars  in Immunopathology [online], 39 (6), 653–667. Available from: https://pubmed.ncbi.nlm.nih.gov/ 29170800/ [Accessed 17 Feb 2021].

Knip, M. and Simell, O., 2012. Environmental Triggers of Type 1 Diabetes. Cold Spring Harbor  Perspectives in Medicine [online], 2 (7). Available from: https://www.ncbi.nlm.nih.gov/pmc/ articles/PMC3385937/#A007690C30.

Lamb, M. M., Myers, M. A., Barriga, K., Zimmet, P. Z., Rewers, M., and Norris, J. M., 2008.  Maternal diet during pregnancy and islet autoimmunity in offspring. Pediatric Diabetes, 9 (2),  135–141.  


Luopajärvi, K., Nieminen, J., Ilonen, J., Åkerblom, H. K., Knip, M., and Vaarala, O., 2012.  Expansion of CD4+CD25+FOXP3+ regulatory T cells in infants of mothers with type 1 diabetes.  Pediatric Diabetes, 13 (5), 400–407.  



Maahs, D. M., West, N. A., Lawrence, J. M., and Mayer-Davis, E. J., 2010. Epidemiology of  Type 1 Diabetes. Endocrinology and Metabolism Clinics of North America [online], 39 (3), 481– 497. Available from: https://www.endo.theclinics.com/article/S0889-8529(10)00043-5/abstract.  


Mayo Clinic, 2020. Type 1 diabetes - Symptoms and causes [online]. Mayo Clinic. Available  from: https://www.mayoclinic.org/diseases-conditions/type-1-diabetes/symptoms-causes/ syc-20353011.  


Michels, A. and Gottlieb, P., 2000. Pathogenesis of Type 1A Diabetes [online]. PubMed.  Available from: https://www.ncbi.nlm.nih.gov/books/NBK279002/ [Accessed 16 Feb 2021].  


Mohammad-Panah, R., n.d. INDEPENDENT RESEARCH PROJECT (in fulfillment of DSHM  Hons The review of the homeopathic concept of susceptibility [online]. Available from: https:// www.homeopathycanada.com/sites/default/files/research-papers/irp-susceptibility.pdf.  


Morrison, J. and Regnault, T., 2016. Nutrition in Pregnancy: Optimising Maternal Diet and Fetal  Adaptations to Altered Nutrient Supply. Nutrients [online], 8 (6), 342. Available from: https:// www.ncbi.nlm.nih.gov/pmc/articles/PMC4924183/.  

Mustonen, N., Siljander, H., Peet, A., Tillmann, V., Härkönen, T., Ilonen, J., Hyöty, H., and Knip,  M., 2017. Early childhood infections precede development of beta-cell autoimmunity and type 1  diabetes in children with HLA-conferred disease risk. Pediatric Diabetes, 19 (2), 293–299.  


National Institute of Diabetes and Digestive and Kidney Diseases, 2019. Monogenic Diabetes  (Neonatal Diabetes Mellitus & MODY) | NIDDK [online]. National Institute of Diabetes and  Digestive and Kidney Diseases. Available from: https://www.niddk.nih.gov/health-information/ diabetes/overview/what-is-diabetes/monogenic-neonatal-mellitus-mody.  


Not Available, N. A., 1999. Vitamin D supplement in early childhood and risk for Type I  (insulin-dependent) diabetes mellitus. Diabetologia, 42 (1), 51–54.  


R. Rughani, Dr. Nirav., 2016. Role of Homoeopathy in Genetic Disorder [online].  www.practo.com. Available from: https://www.practo.com/healthfeed/role-of-homoeopathy-in genetic-disorder-7368/post [Accessed 16 Feb 2021].  

Rewers, M. and Zimmet, P., 2004. The rising tide of childhood type 1 diabetes—what is the  elusive environmental trigger? The Lancet, 364 (9446), 1645–1647.  


Stene, L. C. and Gale, E. A. M., 2013. The prenatal environment and type 1 diabetes.  Diabetologia, 56 (9), 1888–1897.  

Stene, L. C., Ulriksen, J., Magnus, P., and Joner, G., 2000. Use of cod liver oil during pregnancy  associated with lower risk of Type I diabetes in the offspring. Diabetologia, 43 (9), 1093–1098.  


Virtanen, S. M., Kenward, M. G., Erkkola, M., Kautiainen, S., Kronberg-Kippilä, C., Hakulinen,  T., Ahonen, S., Uusitalo, L., Niinistö, S., Veijola, R., Simell, O., Ilonen, J., and Knip, M., 2006.  Age at introduction of new foods and advanced beta cell autoimmunity in young children with  HLA-conferred susceptibility to type 1 diabetes. Diabetologia, 49 (7), 1512–1521.  

Virtanen, S., Uusitalo, L., Kenward, M., Nevalainen, J., Uusitalo, U., Kronberg-Kippilä, C.,  Ovaskainen, M-L., Arkkola, T., Niinistö, S., Hakulinen, T., Ahonen, S., Simell, O., Ilonen, J.,  Veijola, R., and Knip, M., 2010. Maternal food consumption during pregnancy and risk of  advanced β-cell autoimmunity in the offspring. Pediatric Diabetes, 12 (2), 95–99.  


Viskari, H., Knip, M., Tauriainen, S., Huhtala, H., Veijola, R., Ilonen, J., Simell, O., Surcel, H.- M. ., and Hyoty, H., 2012. Maternal Enterovirus Infection as a Risk Factor for Type 1 Diabetes in  the Exposed Offspring. Diabetes Care, 35 (6), 1328–1332.  


Vithoulkas, G., n.d. The Science of Homeopathy, chapter 5, page.75-85.  


Warram, J. H., Krolewski, A. S., Gottlieb, M. S., and Kahn, C. R., 1984. Differences in Risk of  Insulin-Dependent Diabetes in Offspring of Diabetic Mothers and Diabetic Fathers. New  England Journal of Medicine, 311 (3), 149–152.

Back to Top