Diabetes type 1 hereditary


From San Jose, California, USA:

Is diabetes recessive or dominant, and how is it inherited? A lot of my ancestors have diabetes and I wanted to know the chance I would get diabetes.


The inheritance of diabetes is rather more complicated than the simple Mendelian concept of dominant and recessive, autosomal or sex-linked. Type 1 Diabetes depends to some extent on the inherited pattern of certain white blood cell surface proteins, usually referred to as HLA types. However, there is an environmental component which is a major factor in deciding whether those who are ‘at risk’ will develop clinical diabetes. This was realised when it was found that identical twins were discordant for this kind of diabetes. What the factor(s) are is not known: for a number of years early exposure to cow’s milk was thought to be one; but this has subsequently been discounted.

In adult onsetdiabetes, it is even harder to be precise about the likelihood of developing the condition. In some cases especially amongst Maturity Onset Diabetes of the Young specific chromosomal abnormalities have been defined; but there has not been time to assemble the family trees needed to define the actual mode of inheritance. For the majority of Type 2 Diabetics the mechanisms are not defined in precise molecular or chromosomal terms. Ethnic factors are also important.

Finally, there is the factor of stress which may hasten the onset of any form of diabetes and perhaps the commonest of these in later life is age. You write about ‘ancestors’ which suggest that you have no first degree relatives with any form of diabetes. This in turn would suggest that your chances of getting the disease are no more than for the population as a whole, age adjusted.


Original posting 20 Jan 97

Sex-Related Bias and Exclusion Mapping of the Nonrecombinant Portion of Chromosome Y in Human Type 1 Diabetes in the Isolated Founder Population of Sardinia


A male excess in Sardinian type 1 diabetic cases has previously been reported and was largely restricted to those patients carrying the HLA-DR3/nonDR4 genotype. In the present study, we have measured the male- to-female (M:F) ratio in a sample set of 542 newly collected, early-onset type 1 diabetic Sardinian patients. This data not only confirm the excess of male type 1 diabetic patients overall (M:F ratio = 1.3, P = 3.9 × 10−3) but also that the bias in male incidence is largely confined to patients with the DR3/nonDR4 genotype (M:F ratio = 1.6, P = 2.0 × 10−4). These sex effects could be due to a role for allelic variation of the Y chromosome in the susceptibility to type 1 diabetes, but to date this chromosome has not been evaluated in type 1 diabetes. We, therefore, established the frequencies of the various chromosome Y lineages and haplotypes in 325 Sardinian male patients, which included 180 cases with the DR3/nonDR4 genotype, and 366 Sardinian male control subjects. Our results do not support a significant involvement of the Y chromosome in DR3/nonDR4 type 1 diabetic cases nor in early-onset type 1 diabetes as a whole. Other explanations, such as X chromosome-linked inheritance, are thus required for the male bias in incidence in type 1 diabetes in Sardinia.

Type 1 diabetes is the only common autoimmune trait that does not exhibit a strong female excess in the patients. A male excess has been reported in specific subgroups of type 1 diabetic patients, defined by the population of origin, the age of onset of the disease, and the genotypes at the major disease locus, HLA/IDDM1. In early-onset type 1 diabetes, with a diagnosis under the age of 15 years, an increased male-to-female (M:F) ratio was observed in the patients from the high type 1 diabetes risk population of Sardinia (M:F ratio = 1.5) (1). To a lesser extent, the bias is also observed in other high incidence European populations (1). It has been reported that in Sardinia the male excess is largely restricted to those patients carrying the DR3/nonDR4 genotype at the major disease locus, IDDM1. No significant sex effects were observed in the DR4/nonDR3, DR3/4, and nonDR3/nonDR4 categories (2). A male bias is consistently observed in patients diagnosed between the ages of 15 and 40 years from across Europe, but this appears to be independent of HLA type (3). Overall, these observations are consistent with an involvement of the sex chromosomes in type 1 diabetes. Suggestive evidence of linkage of type 1 diabetes to chromosome Xp22-p11 has been reported in families with DR3/nonDR4-affected sib-pairs (2). Nevertheless, it is possible that chromosome Y might account, at least in part, for the above described sex effects in type 1 diabetes. Moreover, some nonallelic homologues of genes located on chromosome X are contained in the nonrecombinant portion of chromosome Y (NRY). For instance, chromosome Y encodes a minor histocompatibility antigen (UTY) homologue of (UTX) (4), which is located in the chromosome X interval (Xp22-p11) that showed linkage to type 1 diabetes (2). Despite these observations, chromosome Y is the only portion of the human genome that has never been scanned for its involvement in type 1 diabetes. Exclusion mapping of the Y chromosome for disease association can be carried out by using a relatively low number of markers by virtue of the absence of crossing-over in the NRY. In the present report, we have tested the possibility that the Y chromosome is responsible for the high M:F ratio using a large male case-control sample set from Sardinia.

We have first determined the M:F ratio bias in a sample set of 542 Sardinian patients, diagnosed under age 15 years, analyzed for the first time in the present study (Table 1). The analysis of these newly reported cases provides a clear confirmation that in Sardinian early-onset patients there is a male excess (M:F ratio = 1.3, one-tailed P = 3.9 × 10−3) and that the bias in male incidence is almost exclusively restricted to patients with the DR3/nonDR4 genotype (M:F ratio = 1.6, one-tailed P = 2.0 × 10−4) (Table 1). In particular in this new collection of cases, we found significant heterogeneity, evaluated using a 2 × 2 contingency table and tested by a χ2 test, in the M:F ratios between the DR3/nonDR4 and DR4/nonDR3 genotypes (P = 3.3 × 10−3). These results are similar to those we reported previously in an independent sample set of 325 Sardinian type 1 diabetic subjects (2). We also analyzed the M:F ratio in 471, fully HLA-typed, unaffected siblings of type 1 diabetic patients. We observed an overall M:F ratio of 0.9 with a similar value also in the DR3/nonDR4 category (98 males and 109 females, M:F ratio = 0.9). Thus, there was significant heterogeneity in the M:F ratios in the DR3/nonDR4 category between the affected patients and their unaffected siblings (P = 1.1 × 10−4).

Owing to the strong male excess in patients and the high frequency of HLA-DR3, Sardinia offers a special opportunity to assess if the Y chromosome is involved in the inheritance of type 1 diabetes. We, therefore, evaluated the association of the Y chromosome with type 1 diabetes by using a male case-control sample set from Sardinia of 325 unrelated early-onset male and 366 unrelated male control subjects. The main chromosome Y lineages and haplotypes were established (see research design and methods) and their frequencies contrasted in patients and control subjects (Table 2). The haplotypes shown in Table 2 define 97.3% of the chromosome Y variability present in the general Sardinian population, while the remaining variation is accounted for by a combination of very rare lineages and haplotypes (D.C., F.C., unpublished results). There is no significant association of any chromosome Y marker with type 1 diabetes in this dataset. The Eu10/Eu12 was under-represented in the patients when compared with the control subjects (P = 2.8 × 10−2), but the difference was no longer significant at the 5% level after correction for number of haplotypes compared (n = 8) (Table 2). Importantly, we did not observe any significant difference in the frequencies of the various chromosome Y markers also when the data were stratified according to the genotypes at the HLA-DRB1 and -DQB1 loci, including the DR3/nonDR4 subgroup (Table 2 and data not shown). The power to detect gene effects with an odds ratio ≥2.5 was >95% at P = 5 × 10−3 for all the chromosome Y haplotypes with the exception of Eu7, for which we had 87.9% power to detect such a gene effect (Table 2). For such a gene effect, even considering the sample size of 180 patients carrying the DR3/nonDR4 genotype, we obtain power >95% for all the chromosome Y haplotypes with the exception of Eu10/12 and Eu7, for which we had 86 and 67.4% power, respectively, to detect association at P = 5 × 10−3 (Table 2).

Finally, we evaluated 11 father-affected son-pairs. We reasoned that even if the Y chromosome was contributing to a small portion of the inheritance of type 1 diabetes, these families were most likely to contain a disease-associated variant. However, we found that these father-son pairs carried four different chromosome Y lineages: Eu4 (three pairs), Eu8 (six pairs), Eu9 (one pair), and Eu18 (one pair), the distribution of which did not significantly differ from that observed in the general population. These results contrast with the existence of Sardinian founder mutations involved in monogenic disorders such as Thalassemia (5), Wilson disease (6), and APECED (autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy) (7) and do not support a founder Sardinian chromosome Y polymorphism contributing to the inheritance of type 1 diabetes in these families. Overall, from our data we can conclude that variation at the NRY is unlikely to contribute in a significant way to the inheritance of type 1 diabetes.

Other explanations are, therefore, required to explain the sex effects observed in this common multifactorial disease. A role for chromosome X is suggested by evidence of linkage of type 1 diabetes to Xp22.11 detected in affected sib-pair families from the U.K. and the U.S. (2,8) and, more recently, in families largely of Scandinavian descent (9). However, the explanation for the sex effects observed in type 1 diabetes could be very complex, because the M:F ratio varies in different countries; in general, with more females affected in countries with lower incidence (10). Either the allele frequency of the putative chromosome X causal variant(s) differs among these distinct populations or the population frequencies of interacting loci at other chromosome locations vary (for example, DR3/nonDR4 genotype frequencies show marked differences across distinct ethnic groups). Additionally but not exclusively, interacting environmental factors may vary in prevalence among countries and influence the penetrance of the putative chromosome X variant in the etiology of type 1 diabetes.

Finally, we excluded the possibility that the male excess in type 1 diabetes that we observed in Sardinian children is due to variation in the levels of the sex hormones during puberty. The initial stages of sexual maturity begin after 9 years of age in over 97% of boys (11) while the age of onset of type 1 diabetes in the Sardinian patients averages <8 years (reasearch design and methods). However, since some of our cases were>9 years of age at diagnosis (but <15 years), we also determined the M:F ratio in only those cases who were ≤8 years at disease onset (n = 446, including cases from our first study). In these patients the male bias was even more pronounced, with 265 males and 181 females overall (M:F ratio = 1.5), and 155 males and 77 females in the DR3/nonDR4 category (M:F ratio = 2). The results presented here provide further justification for the identification of genes on chromosome X that contribute to type 1 diabetes inheritance.


Sample selection.

The total number of type 1 diabetes cases studied from Sardinia was 867, of which 325 were studied previously (2) and 542 were new and unrelated to the previous cases. The average age of the patients at disease onset was 7.8 years, SD ±3.8 years (minimum 0.5 maximun 14); 87.1% of the patients were from the province of Cagliari, 4.2% were from the province of Sassari, 4.3% were from the province of Nuoro, and 4.3% were from the province of Oristano. The involvement of chromosome Y has been examined in a sample set consisting of 325 unrelated male type 1 diabetic patients (selected from the total sample set of 867 patients) and 366 unrelated male control subjects. The average age of onset of these male patients was 7.9 years, SD ±3.9 years (minimum 0.5, maximum 14). The 366 Sardinian control samples were collected from 155 healthy adult male blood donors and 211 newborns that were referred to our center for neonatal screening programs. To restrict the analysis to individuals whose descent was from Sardinia, the surnames of both the patients and control subjects were considered by using the software gens (www.gens.labo.net).

The DNA from the type 1 diabetic patients and the blood donors was prepared from peripheral blood and purified by using a standard salting-out procedure. The DNA from the newborn samples was extracted from dried blood spots of the Guthrie Cards by using the Chelex method (Chelex 100; Bio-Rad, Hercules, CA) (12).

Genotyping and statistical analysis of the data.

The HLA class II typing has been performed as previously described (13). The M:F distribution and M:F ratios were examined in the patients carrying the four main HLA genotype/categories (DR3/nonDR4, DR3/DR4, DR4/nonDR3, and nonDR3/nonDR4) as well as in the patients unstratified by HLA genotype. The P values were one-tailed based on our prior observations (2) and computed using a 2 × 1 contingency table versus a null hypothesis of equal distribution of males and females in each category (Table 1).

Male samples of 325 type 1 diabetic patients and 366 control subjects were then typed for nine chromosome Y diallelic polymorphisms and one Alu insertion (Yap) located in the NRY selected for their European-specific distribution sample (14). We used a step-wise genotyping approach based on the relative frequencies of the various chromosome Y markers obtained from a previous analysis on a smaller Sardinian sample (14). Since phylogenetically assessed, these polymorphisms were classified by Underhill et al. (15) in order of descent and called M1, M9, M26, M35, M89, M170, M172, M173, and M201. M1 (YAP) was typed by using the method of Hammer and Horai (16). M9 and M35, were typed by restriction fragment-length polymorphism using HinfI and BrsI, respectively (15); the M89 and M170 single-nucleotide polymorphisms with an amplification refractory mutation system PCR (17). Dot Blot analysis was used for M26 and M173. M201 and M172 were typed by using the transgenomic system for denaturing high-performance liquid chromatography analysis (18). Primers and probes used in this study are shown in Table 3.

The distribution of the patient and control lineages and haplotypes, determined with a gene counting procedure, was then arranged in a 2 × 2 contingency table and tested by Fisher’s exact or Pearson’s χ2 test and the ORs were computed. The statistical power of our sample set has been computed considering the individual frequencies in the general population of the various lineages and haplotypes based on standard epidemiological measures applied to 2 × 2 contingency tables. We based our power calculations on a gene effect with OR = 2.5, a value comparable to the OR observed for the class I VNTR allele at INS/IDDM2 on chromosome 11p15.

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M:F ratio in 542 early-onset type 1 diabetic patients from Sardinia according to the HLA/IDDM1 genotypes

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The distribution of chromosome Y haplotypes in 325 Sardinian early-onset type 1 diabetic patients and in 366 ethnically matched control subjects

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List of primers and probes redesigned for this study


F.C. and J.A.T. are recipients of a Wellcome Trust Biomedical Research Collaboration Grant. We thank the Italian Telethon, the Juvenile Diabetes Research Foundation, the Regione Autonoma Sardegna Assessorato Sanita’, and the Wellcome Trust for financial support.

Thanks to Antonio Cao for continuous support and encouragement. We also thank Michael Whalen, Mauro Congia, M. Antonietta Asunis, and Mario Silvetti for help and advice; Heather Cordell for statistical advice; Margi Chessa and Rossella Ricciardi for help in collecting the Sardinian type 1 diabetic family and clinical information; and Maria Melis and Antonella Deidda for taking the blood of the patients and their relatives.


  • Address correspondence and reprint requests to Francesco Cucca, Dipartimento di Scienze Biomediche e Biotecnologie, University of Cagliari, Via Jenner, Cagliari 09121, Italy. E-mail: fcucca{at}mcweb.unica.it.

    Received for publication 10 June 2002 and accepted in revised form 26 August 2002.

    D.C. and L.M. contributed equally to this article.

    M:F, male-to-female; NRY, nonrecombinant portion of chromosome Y.

  1. ↵ Karvonen M, Viik-Kajander M, Moltchanova E, Libman I, LaPorte R, Tuomilehto J: Incidence of childhood type 1 diabetes worldwide: Diabetes Mondiale (DiaMond) Project Group. Diabetes Care23 :1516 –1526,2000
  2. ↵ Cucca F, Goy JV, Kawaguchi Y, Esposito L, Merriman ME, Wilson AJ, Cordell HJ, Bain SC, Todd JA: A male-female bias in type 1 diabetes and linkage to chromosome Xp in MHC HLA-DR3-positive patients. Nat Genet19 :301 –3021998
  3. ↵ Weets I, Van Autreve J, Van der Auwera BJ, Schuit FC, Du Caju MV, Decochez K, De Leeuw IH, Keymeulen B, Mathieu C, Rottiers R, Dorchy H, Quartier E, Gorus FK: Male-to-female excess in diabetes diagnosed in early adulthood is not specific for the immune-mediated form nor is it HLA-DQ restricted: possible relation to increased body mass index. Diabetologia44 :40 –47,2001
  4. ↵ Vogt MH, Goulmy E, Kloosterboer FM, Blokland E, de Paus RA, Willemze R, Falkenburg JH: UTY gene codes for an HLA-B60-restricted human male-specific minor histocompatibility antigen involved in stem cell graft rejection: characterization of the critical polymorphic amino acid residues for T-cell recognition. Blood96 :3126 –3132,2000
  5. ↵ Rosatelli MC, Dozy A, Faa V, Meloni A, Sardu R, Saba L, Kan YW, Cao A: Molecular characterization of beta-thalassemia in the Sardinian population. Am J Hum Genet50 :422 –426,1992
  6. ↵ Loudianos G, Dessi V, Lovicu M, Angius A, Figus A, Lilliu F, De Virgiliis S, Nurchi AM, Deplano A, Moi P, Pirastu M, Cao A: Molecular characterization of wilson disease in the Sardinian population-evidence of a founder effect. Hum Mutat14 :294 –303,1999
  7. ↵ Rosatelli MC, Meloni A, Devoto M, Cao A, Scott HS, Peterson P, Heino M, Krohn KJ, Nagamine K, Kudoh J, Shimizu N, Antonarakis SE: A common mutation in Sardinian autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy patients. Hum Genet103 :428 –434,1998
  8. ↵ Cordell HJ, Kawaguchi Y, Todd JA, Farrall M: An extension of the maximum lod score method to X-linked loci. Ann Hum Genet59 :435 –449,1995
  9. ↵ Nerup J, Pociot F: A genomewide scan for type 1-diabetes susceptibility in Scandinavian families: identification of new loci with evidence of interactions. Am J Hum Genet69 :1301 –1313,2001
  10. ↵ Karvonen M, Pitkaniemi M, Pitkaniemi J, Kohtamaki K, Tajima N, Tuomilehto J: Sex difference in the incidence of insulin-dependent diabetes mellitus: an analysis of the recent epidemiological data. World Health Organization DIAMOND Project Group. Diabetes Metab Rev13 :275 –291,1997
  11. ↵ Tanner JM, Davies PS: Clinical longitudinal standards for height and height velocity for North American children. J Pediatr107 :317 –329,1985
  12. ↵ Walsh PS, Metzger DA, Higuchi R: Chelex 100 as a medium for simple extraction of DNA for PCR-based typing from forensic material. Biotechniques10 :506 –513,1991
  13. ↵ Cucca F, Lampis R, Frau F, Macis D, Angius E, Masile P, Chessa M, Frongia P, Silvetti M, Cao A, et al: The distribution of DR4 haplotypes in Sardinia suggests a primary association of type I diabetes with DRB1 and DQB1 loci. Hum Immunol43 :301 –308,1995
  14. ↵ Semino O, Passarino G, Oefner PJ, Lin AA, Arbuzova S, Beckman LE, De Benedictis G, Francalacci P, Kouvatsi A, Limborska S, Marcikiae M, Mika A, Mika B, Primorac D, Santachiara-Benerecetti AS, Cavalli-Sforza LL, Underhill PA: The genetic legacy of Paleolithic Homo sapiens sapiens in extant Europeans: a Y chromosome perspective. Science290 :1155 –1159,2000
  15. ↵ Underhill PA, Shen P, Lin AA, Jin L, Passarino G, Yang WH, Kauffman E, Bonne-Tamir B, Bertranpetit J, Francalacci P, Ibrahim M, Jenkins T, Kidd JR, Mehdi SQ, Seielstad MT, Wells RS, Piazza A, Davis RW, Feldman MW, Cavalli-Sforza LL, Oefner PJ: Y chromosome sequence variation and the history of human populations. Nat Genet26 :358 –361,2000
  16. ↵ Hammer MF, Spurdle AB, Karafet T, Bonner MR, Wood ET, Novelletto A, Malaspina P, Mitchell RJ, Horai S, Jenkins T, Zegura SL: The geographic distribution of human Y chromosome variation. Genetics145 :787 –805,1997
  17. ↵ Powis SH, Tonks S, Mockridge I, Kelly AP, Bodmer JG, Trowsdale J: Alleles and haplotypes of the MHC-encoded ABC transporters TAP1 and TAP2. Immunogenetics37 :373 –380,1993
  18. ↵ Underhill PA, Jin L, Lin AA, Mehdi SQ, Jenkins T, Vollrath D, Davis RW, Cavalli-Sforza LL, Oefner PJ: Detection of numerous Y chromosome biallelic polymorphisms by denaturing high-performance liquid chromatography. Genome Res7 :996 –1005,1997

Sex-linked recessive

Sex-linked diseases are passed down through families through one of the X or Y chromosomes. X and Y are sex chromosomes.

Dominant inheritance occurs when an abnormal gene from one parent causes disease, even though the matching gene from the other parent is normal. The abnormal gene dominates.

But in recessive inheritance, both matching genes must be abnormal to cause disease. If only one gene in the pair is abnormal, the disease does not occur or it is mild. Someone who has one abnormal gene (but no symptoms) is called a carrier. Carriers can pass abnormal genes to their children.

The term “sex-linked recessive” most often refers to X-linked recessive.

X-linked recessive diseases most often occur in males. Males have only one X chromosome. A single recessive gene on that X chromosome will cause the disease.

The Y chromosome is the other half of the XY gene pair in the male. However, the Y chromosome doesn’t contain most of the genes of the X chromosome. Because of that, it doesn’t protect the male. Diseases such as hemophilia and Duchenne muscular dystrophy occur from a recessive gene on the X chromosome.


In each pregnancy, if the mother is a carrier of a certain disease (she has only one abnormal X chromosome) and the father is not a carrier for the disease, the expected outcome is:

  • 25% chance of a healthy boy
  • 25% chance of a boy with disease
  • 25% chance of a healthy girl
  • 25% chance of a carrier girl without disease

If the father has the disease and the mother is not a carrier, the expected outcomes are:

  • 100% chance of a healthy boy
  • 100% chance of a carrier girl without disease


Females can get an X-linked recessive disorder, but this is very rare. An abnormal gene on the X chromosome from each parent would be required, since a female has two X chromosomes. This could occur in the two scenarios below.

In each pregnancy, if the mother is a carrier and the father has the disease, the expected outcomes are:

  • 25% chance of a healthy boy
  • 25% chance of a boy with the disease
  • 25% chance of a carrier girl
  • 25% chance of a girl with the disease

If both the mother and the father have the disease, the expected outcomes are:

  • 100% chance of the child having the disease, whether boy or girl

The odds of either of these two scenarios are so low that X-linked recessive diseases are sometimes referred to as male only diseases. However, this is not technically correct.

Female carriers can have a normal X chromosome that is abnormally inactivated. This is called “skewed X-inactivation.” These females may have symptoms similar to those of males, or they may have only mild symptoms.

Genetics is the study of heredity and how traits are passed along from parents to offspring. Genes are contained within the chromosomes found within the egg and sperm. Each parent contributes one half of each pair or 23 chromosomes to their child, 22 autosomal and 1 sex chromosome. The inheritance of genetic diseases, abnormalities, or traits is described by both the type of chromosome the abnormal gene resides on (autosomal or sex chromosome), and by whether the gene itself is dominant or recessive.

Can Diabetes Be Prevented?

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What Is Diabetes?

Diabetes is a disease that affects how the body uses glucose, the main type of sugar in the blood. Glucose, which comes from the foods we eat, is the major source of energy needed to fuel the body. To use glucose, the body needs the hormone insulin. But in people with diabetes, the body either can’t make insulin or the insulin doesn’t work in the body like it should.

The two major types of diabetes are:

  1. Type 1 diabetes, in which the immune system attacks the pancreas and destroys the cells that make insulin.
  2. Type 2 diabetes, in which the pancreas can still make insulin, but the body doesn’t respond to it properly.

In both types of diabetes, glucose can’t get into the cells normally. This causes a rise in blood sugar levels, which can make someone sick if not treated.

Can Type 1 Diabetes Be Prevented?

Type 1 diabetes can’t be prevented. Doctors can’t even tell who will get it and who won’t.

No one knows for sure what causes type 1 diabetes, but scientists think it has something to do with genes. But just getting the genes for diabetes isn’t usually enough. In most cases, a child has to be exposed to something else — like a virus — to get type 1 diabetes.

Type 1 diabetes isn’t contagious, so kids and teens can’t catch it from another person or pass it along to friends or family members. And eating too much sugar doesn’t cause type 1 diabetes, either.

There’s no reliable way to predict who will get type 1 diabetes, but blood tests can find early signs of it. These tests aren’t done routinely, however, because doctors don’t have any way to stop a child from developing the disease, even if the tests are positive.

Can Type 2 Diabetes Be Prevented?

Unlike type 1 diabetes, type 2 diabetes can sometimes be prevented. Excessive weight gain, obesity, and a sedentary lifestyle are all things that put a person at risk for type 2 diabetes.

In the past, type 2 diabetes usually happened only in adults. But now, more kids and teens are being diagnosed with type 2 diabetes, due to the rapidly increasing number of overweight kids.

Although kids and teens might be able to prevent or delay the onset of type 2 diabetes by managing their weight and increasing physical activity, other risk factors for type 2 diabetes can’t be changed. Kids with one or more family members with type 2 diabetes have an increased risk for the disease, and some ethnic and racial groups are more likely to developing it.

How Can I Protect My Kids From Developing Type 2 Diabetes?

These steps can help reduce your kids’ risk for developing type 2 diabetes and the health problems it can cause:

  • Make sure kids eat a healthy diet. Encouraging your kids to eat low-fat, nutrient-rich foods — like whole-grain cereals and breads, fruits, vegetables, dairy products, and lean proteins — can help prevent excessive weight gain, a major risk factor for type 2 diabetes.
  • Limit sugary foods and beverages. Consuming lots of sugar-filled foods and beverages — like sodas, juices, and iced teas — can lead to excessive weight gain.
  • Encourage lots of physical activity. Staying active and limiting the time spent in sedentary activities — like watching TV, being online, or playing video or computer games — can help reduce the risk of weight gain and help prevent the onset of type 2 diabetes. Being active can be as simple as walking the dog or mowing the lawn. Try to do something that gets you and your kids moving every day.

If you think your child may be overweight and at risk for type 2 diabetes, talk to your doctor or a registered dietitian. They can help you learn what your child’s weight goals should be and how to reach them.

Reviewed by: Steven Dowshen, MD Date reviewed: February 2018

  1. Although you inherit diabetes, it skips a generation.Not everyone who gets diabetes inherits it. You may have no relatives with diabetes or several. Also, diabetes doesn’t skip a generation, nor are you more likely to get it from either your mother or father. Both your genes and your lifestyle contribute to your risk for diabetes. And, it doesn’t come from eating too much sugar.
  2. People with diabetes shouldn’t eat carrots because they are high in sugar.
    Like all vegetables, carrots are carbohydrates. Carbohydrates are part of a healthy diet and help give you the energy, vitamins and minerals your body needs to function. All carbohydrates affect your blood sugar the same amount, whether you are getting the same amount of carbohydrate in bread, pasta, sugar or vegetables. Three cups of uncooked and 1 and 1/2 cup of cooked carrots will raise your blood sugar the same amount as 1 slice of bread. And just to clear up another myth, people with diabetes can eat sugar as part of their meal plan.
  3. I don’t have to worry, I just have borderline diabetes.
    There really is no such thing as borderline diabetes. You either have diabetes, pre-diabetes, or no diabetes. Fasting blood sugar readings of greater than 126 mg/dl or more than one occasion are considered diabetes. A fasting blood sugar of 110-125 mg/dl on more than one occasion is considered pre-diabetes. Pre-diabetes is a strong risk factor for developing type 2 diabetes.
  4. There is nothing you can do to keep from getting diabetes.
    We have learned recently that you can prevent diabetes at any age. In fact, losing a modest amount of weight (5-10% of your total weight), being moderately active (by walking or doing other forms of exercise for 150 minutes per week) can delay or prevent the onset of type 2 diabetes.
  5. You should never use herbal or natural remedies when you have diabetes.
    The most natural of remedies is eating a healthy diet and exercise. Medically-proven diabetes information shows that both meal planning and activity help to lower your blood sugar levels. Combining your prescribed medicines with a meal plan and physical activity gives you the most for your money. It is true that some herbal or other products can work against your diabetes medicines, may raise your blood sugar or may even be dangerous. Ask your pharmacist or health care provider if any of your medicines or health problems are affected by the herbal or vitamin products you take.
  6. Insulin causes complications, such as amputations, impotence or even death.
    Some people who take insulin develop complications from diabetes, but the complications aren’t caused by insulin. Keeping your blood sugar near the normal range by using a pills or insulin helps you to live a long and healthy life. Also many people believe that once you start taking insulin, you can never stop. While this used to be true, the insulin that is on the market today is better than in the past.
  7. You can’t get off of insulin.
    Some people with type 2 diabetes are able to stop taking insulin if they lose weight, start exercising or if the physical or emotional stress that raised their blood sugar is better.
  8. It’s a good idea for people with diabetes to soak their feet in vinegar every day.
    Many years ago, people with diabetes were told to soak their feet every day. We know now that soaking with water, vinegar and other products can make your skin dry – which can cause cracks in the skin where bacteria can enter.
  9. I feel fine as long as my blood sugar is less than 250.
    Isn’t that “normal” for me? Not really. Your usual blood sugar isn’t the same as normal blood sugar. Just because your blood sugar is usually high or you don’t notice any symptoms, does not mean that your body is not being affected by those levels.
  10. I don’t have to worry about my children getting diabetes until they are adults.
    Sadly, more and more young people are getting type 2 diabetes. It is caused from a combination of being overweight, getting less exercise and heredity. You can help your children and grandchildren prevent diabetes by encouraging them to keep active and stay at a reasonable weight.

About type 2 diabetes

Type 2 diabetes is the most common form of diabetes. Most of the people with diabetes in the United States have type 2 diabetes, and it is on the rise, especially in younger people. More preteens, teens, and young adults are being diagnosed with type 2 diabetes than ever before.


Like type 1 diabetes, type 2 diabetes is inherited. This means a group of genes that can lead to type 2 is passed down from mothers and fathers to their children. Not everyone who inherits the genes will develop it, but if you have the genes for type 2 diabetes, you’ve got a greater chance of developing it. Your chances are even higher if you’re also overweight and don’t get much exercise.

Having a sweet tooth won’t cause type 2 diabetes, but a diet high in simple sugars and other unhealthy foods can cause you to gain weight. Most people who are diagnosed with type 2 diabetes are overweight.

In addition to being overweight, there are some other factors that put a person at a higher risk for developing type 2 diabetes, including:

  • Having a family history of diabetes.
  • Being older than 40.
  • Having gestational diabetes during a pregnancy.
  • Giving birth to a baby weighing more than 9 pounds.
  • Being African American, Hispanic American, Asian American, or Native American.

Insulin resistance and impaired fasting glucose

Insulin resistance is when cells have trouble using insulin. The cells resist insulin’s message to open up, and don’t work as fast to let the sugar in. When this happens, the pancreas works harder to make more insulin, which it releases into the blood to keep blood sugar levels normal.

Insulin resistance can lead to a condition called impaired glucose tolerance or impaired fasting glucose. This happens when the pancreas can’t make enough insulin to keep blood sugar levels in a normal range.

  • In someone with normal glucose tolerance, the fasting blood glucose (the blood test done first thing in the morning before a person eats anything) is always less than 100.
  • A person with impaired glucose tolerance has a fasting blood glucose level between 100 and 125.
  • A person has diabetes when his or her fasting blood glucose is always higher than 125.


The symptoms of type 2 diabetes can develop slowly over time. Sometimes they’re mistaken for other health problems. Because symptoms show up slowly, it’s estimated that about eight million people in the United States have type 2 diabetes and don’t know it.

These signs of type 2 diabetes will appear when a person’s blood sugar is high and stays high:

  • Fatigue. The body isn’t able to convert sugar from food into energy.
  • Urinating more than usual. The kidneys are getting rid of the extra sugar in the blood through the urine.
  • Extreme thirst. The body loses lots of water through more urination.
  • Prone to infections. Watch for vaginal infections or skin wounds that heal slowly.
  • Dehydration. The body keeps losing water from increased urination.
  • Dry, itchy skin. This can happen from being dehydrated.
  • Numbness or tingling in hands or feet. Over time, high blood-sugar levels affect the nerves that allow us to feel pressure, pain, and hot and cold.
  • Blurred eyesight. The lenses of the eyes swell with fluid.
  • Problems having sex. The sex organs are affected by lack of blood flow.


Each person with type 2 diabetes will have a care plan designed to address his or her specific health problems and meet their goals. One person’s treatment plan won’t be same as anyone else’s. Additionally, a person’s care plan can change over time as needs change.

A small number of people with type 2 diabetes can keep their blood sugar levels in a normal range by following a care plan that involves watching what they eat, getting physical activity, and staying at a healthy weight. This is especially true for people who are diagnosed in the early stages of diabetes, while their bodies are still making insulin.

Many people who don’t start out taking medicine, begin taking medicine after having diabetes for awhile. People sometimes start on diabetes pills to help their bodies use its own insulin better. When pills aren’t enough, a person might start to take a shot of insulin before bed or at other times during the day.

When a person is asked to start diabetes pills or insulin as part of his or her care plan, it’s usually not because the person did something wrong. It’s just the next step in helping to gain better control of blood sugar levels.


Having insulin resistance or impaired glucose tolerance can increase your chances of developing diabetes in the future. But there are things you can do to lower your risk.

You can help your body’s cells respond better to insulin by maintaining a healthier weight and getting regular exercise. With less resistance, insulin can move sugar into your cells faster, and your pancreas won’t have to work so hard to keep up with your body’s demands for insulin.

If you’re at risk for type 2 diabetes, you might be able to delay or prevent it with good habits, including a healthy diet, regular exercise, and if needed, losing weight.

Clinical review by Avantika Waring, MD
Kaiser Permanente
Reviewed 01/03/2019

Diabetes and Family History: How Much Risk is Genetic?

Whether you have Type I or Type II diabetes, there are several factors that could have contributed to the disease. Among these are your family’s lifestyle and your genetic history. By gaining a better understanding of these two issues, you may be able to control your diabetes with more ease, or possibly (in the case of Type II) avoid it altogether. At the very least, understanding the risks created by your genetic and family history will allow you to detect diabetes earlier and avoid the damage it can do if left untreated.

How Family Affects Diabetes Risk

Your family affects your diabetes risk in two different ways. First, of course, your parents contributed to your genetic heritage. But there’s also the way your parents, your siblings, and your extended family may have influenced the way you eat, exercise, and care for yourself, because these are habits you learn from the people around you as you grow up. Your genetic makeup can play a big role in both Type I and Type II diabetes, while the way a family cares for itself and the habits you’re taught in regard to diet and exercise are generally more related to Type II risk.

To help prevent Type II diabetes if you don’t have the disease yet or if you’re prediabetic, there are four questions the NIDDK suggests you ask your family. These are:

  • Does anyone in your family have Type II diabetes and if so, who are they?
  • Has anyone in your family been told they may develop diabetes or are at risk for it?
  • Has anyone in your family been told they need to get more exercise or lose weight in order to prevent diabetes?
  • Did your mother have diabetes when she was pregnant, either with me or with a sibling?

Type II diabetes can be greatly affected by the lifestyle a family lives. As you grow up and get older you learn a lot of habits from your family. If these are bad habits—if you don’t see the people around you exercising, eating healthy food, or maintaining a healthy weight, the odds are higher that you will also struggle with obesity, and find yourself at risk for Type II diabetes and the complications that come with it.

By making healthy changes to your weight, diet, and exercise levels, you can reduce the chances of getting Type II diabetes and even reverse it if you already have it. But your family history is important, and asking the right questions can help you make better choices for the future.

Type I diabetes doesn’t have the same kind of relationship to self-care, eating habits, weight, and exercise. It develops in childhood, usually from an autoimmune response that attacks the cells that produce insulin, making it difficult or impossible for the body to process sugar. There’s nothing about how much a person weighs, what they eat, or how much they exercise that will reverse or reduce the risk of Type I diabetes. Still, while staying healthy won’t cure Type I, being aware of the health habits you inherited from your family may help you stay healthier over time.

Genetic Traits and Diabetes Development

Diabetes can come from genetics, just like it can come from family habits. But this is more often a factor in Type I diabetes. If you have family members who have Type I, your risk goes up simply because you carry the same or similar genes. If you or your child has this genetic heritage, be sure to let your doctor know. Make sure, too, that you’re keeping an eye on blood sugar levels and looking out for other symptoms. If you do develop diabetes, then at the very least your family history should allow you treat this illness as soon as it happens, potentially preventing some of the worst complications.

At the same time, understand that having parents or other family members with diabetes, even if both parents or a sibling have the condition, does not guarantee you’ll develop it. This is true for both Type I and Type II diabetes. When an identical twin has Type I diabetes, for example, the American Diabetes Association states that the other twin will only have it a maximum of 50% of the time. When a twin has Type II diabetes, the risk to the other twin is no higher than 75%. It is clear that genetics play a role, but there are factors you can control that will reduce your risk, too.

While you’re not guaranteed to get diabetes if your family has it, and some people with no obvious risk factors still develop it, paying attention to your genetic profile can help you avoid or reduce problems with diabetes and other chronic health conditions. When you address your lifestyle and remain mindful of your genetics, you have the opportunity to take better control of factors you can change, and that can make a big difference for your long-term health and well-being.

Causes of type 1 diabetes

It is important to know it is not your fault that you have type 1 diabetes – it is not caused by poor diet or an unhealthy lifestyle. In fact, it isn’t caused by anything that you did or didn’t do, and there was nothing you could have done to prevent it.

What causes type 1 diabetes?

Because the precise causes of type 1 diabetes are not known and there is a much greater awareness of type 2 diabetes, many myths about type 1 diabetes are in circulation. There has been a lot of research into what causes type 1 diabetes, but so far there are no clear answers.

Type 1 is an autoimmune condition. An autoimmune condition is when your immune system, which normally keeps your body safe against disease, attacks itself instead. Other examples of autoimmune conditions include multiple sclerosis (MS) and rheumatoid arthritis. In type 1 diabetes, the immune system attacks and destroys your insulin-producing beta cells.

Certain genes put people at a greater risk for developing type 1 diabetes, but are not the only factors involved. While there are no proven environmental triggers, researchers are looking for possible culprits, such as viral infections and particular molecules within our environment and foods.

Is type 1 diabetes hereditary?

We are also unsure about whether type 1 diabetes is hereditary or not. While 90 per cent of people who develop type 1 diabetes have no relative with the condition, genetic factors can pre-dispose people to developing type 1 diabetes.

Certain gene markers are associated with type 1 diabetes risk. A child born with these will have the same risk of developing type 1 diabetes as a child with siblings with type 1 diabetes. However, having the marker alone is not enough to cause someone to develop type 1 diabetes – it is thought that an additional trigger causes type 1 diabetes to develop.

About type 1 diabetes

Type 1 diabetes is less common than type 2 diabetes. In the past, type 1 diabetes was called juvenile diabetes, juvenile-onset diabetes, or insulin-dependent diabetes. Today we realize those terms aren’t accurate.

People can develop type 1 as adults, children can develop type 2, and people with type 2 might need to take insulin shots.

Type 1 diabetes is known as an autoimmune disease. It happens because a person’s immune system destroys the body’s beta cells, which make insulin and release it into the blood stream. These cells are located in an organ called the pancreas. When the immune system destroys the beta cells, the body stops being able to make insulin.

Signs of type 1 diabetes start to show up when half or more of the beta cells have been destroyed. People who have type 1 diabetes will begin to take insulin shots right away, to replace the insulin their bodies no longer make.

Type 1 diabetes is inherited, which means a group of genes that can lead to type 1 diabetes is passed down from mothers and fathers to their children. A person with a parent, brother, or sister with type 1 diabetes has a greater chance of also developing type 1 diabetes.

Genes play an important role in determining who gets type 1 diabetes and who doesn’t. But they might not be the only influence. Environmental factors, including viruses and allergies, appear to trigger type 1 diabetes in some people who have inherited the genes.

These factors can trigger type 1 diabetes at any point in a person’s life. That’s why some people don’t develop type 1 diabetes until they’re adults, while others develop it when they’re children.

The symptoms for type 1 diabetes usually show up over a few days or even a few weeks and are caused by high levels of sugar in the blood.

Symptoms include:

  • Urinating more than usual. The kidneys are getting rid of the extra sugar in the blood through the urine.
  • Being very thirsty. The body loses lots of water through more urination.
  • Fatigue. The body isn’t able to convert sugar from food into energy.
  • Hunger. Because the body isn’t getting energy from food, it thinks it’s starving.
  • Serious weight loss. The body burns stored fat and protein to get energy.
  • Nausea and headaches. When blood sugar gets very high, the body breaks down fat, releasing acids into the bloodstream. This is a condition called diabetic ketoacidosis (DKA).
  • Dehydration. The body keeps losing water from increased urination.

When a person gets a diagnosis of type 1 diabetes, he or she needs to immediately replace the insulin that the body isn’t making. This means daily insulin shots, which are timed with meals and snacks — what, when, and how much the person eats — as well as with the person’s exercise and other physical activity.

To know how much insulin you need, or when and how much to eat, you will check blood sugar levels every day. It’s common for people with type 1 diabetes to check their blood sugar levels several times a day, including before or after meals and at bedtime.

While we’re still learning about the genes and other factors that cause type 1 diabetes, we don’t know how to keep people from getting it. Researchers are doing a better job of figuring out who is at risk of developing type 1 diabetes by looking at the level of certain antibodies in a person’s blood. People with higher levels of some of these antibodies have a greater chance of developing type 1 diabetes because these antibodies show that the person’s immune system might be attacking the beta cells in the pancreas.

The goal for preventing type 1 diabetes is to get the body to stop destroying its beta cells. Current studies are exploring whether giving insulin to people at risk for type 1 diabetes can prevent it from developing.

Type 1 diabetes is a lifelong condition. Good lifestyle habits and self-management (keeping blood sugar levels near normal) can help a person with type 1 diabetes stay healthier longer without having many other health problems related to diabetes.

Clinical review by Avantika Waring, MD
Kaiser Permanente
Reviewed 01/03/2019

Does type 2 diabetes run in families?

Unlike some traits, diabetes does not seem to be inherited in a simple pattern. Yet clearly, some people are born more likely to get diabetes than others.

Type 1 and type 2 diabetes have different causes. Yet two factors are important in both. You inherit a predisposition to the disease then something in your environment triggers it.

Genes alone are not enough. One proof of this is identical twins. Identical twins have identical genes. Yet when one twin has type 1 diabetes, the other gets the disease at most only half the time. When one twin has type 2 diabetes, the other’s risk is at most 3 in 4.

Type 2 diabetes has a stronger link to family history and lineage than type 1, although it too depends on environmental factors. Studies of twins have shown that genetics play a very strong role in the development of type 2 diabetes. Lifestyle also influences the development of type 2 diabetes. Obesity tends to run in families, and families tend to have similar eating and exercise habits.

If you have a family history of type 2 diabetes, it may be difficult to figure out whether your diabetes is due to lifestyle factors or genetic susceptibility. Most likely it is due to both. However, don’t lose heart. Studies show that it is possible to delay or prevent type 2 diabetes by exercising and losing weight.

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