Bridging the Gap between Life Insurer and Consumer in the Genetic Testing Era: The RF Proposal

Indiana Law Journal

Volumn 74, Issue 4, 1999, Pages 1375-1392

  Keefer, Christopher M ^a  

^a INDIANA UNIVERSITY   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

ARTICLE; GENETIC PREDISPOSITION; GENETIC PRIVACY; GENETIC SCREENING; GENETICS AND REPRODUCTION; GOVERNMENT; HUMAN; INSURANCE; LEGAL APPROACH; LEGAL ASPECT; RISK; SOCIAL PSYCHOLOGY; UNITED STATES;

GENETICS AND REPRODUCTION; LEGAL APPROACH;

GENETIC PREDISPOSITION TO DISEASE; GENETIC PRIVACY; GENETIC SCREENING; HUMANS; INSURANCE SELECTION BIAS; INSURANCE, LIFE; PREJUDICE; RISK; UNITED STATES; UNITED STATES DEPT. OF HEALTH AND HUMAN SERVICES;

EID: 0033449717     PISSN: 00196665     EISSN: None     Source Type: Journal    
DOI: None     Document Type: Article

References (167)

1. The HGP is a multibillion dollar initiative designed to map and sequence the genes in the human genome. See Heather McClure, The Insurance Industry's Use of Genetic Information: Legal and Ethical Concerns, 28 J. HEALTH & HOSP. L. 231, 231 (1995); Lori Whittaker, Clinical Applications of Genetic Testing: Implications for the Family Physician, 53 AM. FAM. PHYSICIAN 2077, 2077 (1996), available in LEXIS, GENMED Library, AFP File. The genome of an organism consists of its haploid set of chromosomes. Humans have 23 pairs of chromosomes (or 46 total chromosomes). The 23 pairs of chromosomes are known as a diploid set of chromosomes. Each parent donates one set of chromosomes from the pair (known as a haploid set) to the offspring, giving it a diploid set (one haploid set from each parent). Genes are located on each haploid set and are responsible for bodily functions. The HGP is focused on finding the location of human genes on each chromosome in the haploid set. See JAMES W. FRISTROM & PHILIP T. SPIETH, PRINCIPLES OF GENETICS 47, 132-33 (1980); NATIONAL CANCER INST., U.S. DEP'T OF HEALTH AND HUMAN SERVS., UNDERSTANDING GENE TESTING 2 (1995).
2. The HGP is a multibillion dollar initiative designed to map and sequence the genes in the human genome. See Heather McClure, The Insurance Industry's Use of Genetic Information: Legal and Ethical Concerns, 28 J. HEALTH & HOSP. L. 231, 231 (1995); Lori Whittaker, Clinical Applications of Genetic Testing: Implications for the Family Physician, 53 AM. FAM. PHYSICIAN 2077, 2077 (1996), available in LEXIS, GENMED Library, AFP File. The genome of an organism consists of its haploid set of chromosomes. Humans have 23 pairs of chromosomes (or 46 total chromosomes). The 23 pairs of chromosomes are known as a diploid set of chromosomes. Each parent donates one set of chromosomes from the pair (known as a haploid set) to the offspring, giving it a diploid set (one haploid set from each parent). Genes are located on each haploid set and are responsible for bodily functions. The HGP is focused on finding the location of human genes on each chromosome in the haploid set. See JAMES W. FRISTROM & PHILIP T. SPIETH, PRINCIPLES OF GENETICS 47, 132-33 (1980); NATIONAL CANCER INST., U.S. DEP'T OF HEALTH AND HUMAN SERVS., UNDERSTANDING GENE TESTING 2 (1995).
3. The HGP is a multibillion dollar initiative designed to map and sequence the genes in the human genome. See Heather McClure, The Insurance Industry's Use of Genetic Information: Legal and Ethical Concerns, 28 J. HEALTH & HOSP. L. 231, 231 (1995); Lori Whittaker, Clinical Applications of Genetic Testing: Implications for the Family Physician, 53 AM. FAM. PHYSICIAN 2077, 2077 (1996), available in LEXIS, GENMED Library, AFP File. The genome of an organism consists of its haploid set of chromosomes. Humans have 23 pairs of chromosomes (or 46 total chromosomes). The 23 pairs of chromosomes are known as a diploid set of chromosomes. Each parent donates one set of chromosomes from the pair (known as a haploid set) to the offspring, giving it a diploid set (one haploid set from each parent). Genes are located on each haploid set and are responsible for bodily functions. The HGP is focused on finding the location of human genes on each chromosome in the haploid set. See JAMES W. FRISTROM & PHILIP T. SPIETH, PRINCIPLES OF GENETICS 47, 132-33 (1980); NATIONAL CANCER INST., U.S. DEP'T OF HEALTH AND HUMAN SERVS., UNDERSTANDING GENE TESTING 2 (1995).
4. The HGP is a multibillion dollar initiative designed to map and sequence the genes in the human genome. See Heather McClure, The Insurance Industry's Use of Genetic Information: Legal and Ethical Concerns, 28 J. HEALTH & HOSP. L. 231, 231 (1995); Lori Whittaker, Clinical Applications of Genetic Testing: Implications for the Family Physician, 53 AM. FAM. PHYSICIAN 2077, 2077 (1996), available in LEXIS, GENMED Library, AFP File. The genome of an organism consists of its haploid set of chromosomes. Humans have 23 pairs of chromosomes (or 46 total chromosomes). The 23 pairs of chromosomes are known as a diploid set of chromosomes. Each parent donates one set of chromosomes from the pair (known as a haploid set) to the offspring, giving it a diploid set (one haploid set from each parent). Genes are located on each haploid set and are responsible for bodily functions. The HGP is focused on finding the location of human genes on each chromosome in the haploid set. See JAMES W. FRISTROM & PHILIP T. SPIETH, PRINCIPLES OF GENETICS 47, 132-33 (1980); NATIONAL CANCER INST., U.S. DEP'T OF HEALTH AND HUMAN SERVS., UNDERSTANDING GENE TESTING 2 (1995).
5. The HGP is a multibillion dollar initiative designed to map and sequence the genes in the human genome. See Heather McClure, The Insurance Industry's Use of Genetic Information: Legal and Ethical Concerns, 28 J. HEALTH & HOSP. L. 231, 231 (1995); Lori Whittaker, Clinical Applications of Genetic Testing: Implications for the Family Physician, 53 AM. FAM. PHYSICIAN 2077, 2077 (1996), available in LEXIS, GENMED Library, AFP File. The genome of an organism consists of its haploid set of chromosomes. Humans have 23 pairs of chromosomes (or 46 total chromosomes). The 23 pairs of chromosomes are known as a diploid set of chromosomes. Each parent donates one set of chromosomes from the pair (known as a haploid set) to the offspring, giving it a diploid set (one haploid set from each parent). Genes are located on each haploid set and are responsible for bodily functions. The HGP is focused on finding the location of human genes on each chromosome in the haploid set. See JAMES W. FRISTROM & PHILIP T. SPIETH, PRINCIPLES OF GENETICS 47, 132-33 (1980); NATIONAL CANCER INST., U.S. DEP'T OF HEALTH AND HUMAN SERVS., UNDERSTANDING GENE TESTING 2 (1995).
6. Cystic fibrosis ("CF") is one of the most common genetic disorders causing death in the white population. Pulmonary disease is responsible for 90% of CF-related deaths. Liver disease, trauma, and suicide are responsible for the other 5% of CF-related deaths. See generally Garry R. Cutting, Cystic Fibrosis, in 1 EMERY AND RIMOIN'S PRINCIPLES AND PRACTICE OF MEDICAL GENETICS 268 (David L. Rimoin et al. eds., 3d ed. 1997) [hereinafter MEDICAL GENETICS] (discussing symptoms, genetic structure, diagnosis, and management of CF).
7. Huntington's disease ("HD") causes a gradual deterioration of physical and mental capabilities around the age of 40 and lasts for about 15 years, until death. See generally Michael R. Hayden & Barry Kremer, Basal Ganglia Disorders, in 2 MEDICAL GENETICS, supra note 2, at 2197, 2203-09 (discussing symptoms, diagnosis, genetic counseling, and management of Huntington's Disease).
8. Present studies have shown that, although the majority of breast and ovarian cancers develop sporadically, a small percentage (approximately 5-10%) of these cancers are genetically related. See generally C. Michael Steel, Cancer of the Breast and Female Reproductive Tract, in 1 MEDICAL GENETICS, supra note 2, at 1501, 1501-23 (discussing the genetic mapping of heritable breast cancer).
9. Alzheimer's disease is different from other genetically related diseases in that there are different copies of the same gene. If one of the copies of the gene is received from the parent, the process of Alzheimer's is hastened. See generally Allen D. Roses & Margaret A. Pericak-Vance, Alzheimer Disease and Other Dementias, in 2 MEDICAL GENETICS, supra note 2, at 1807, 1807-20 (discussing symptoms, diagnosis, genetic counseling, and management of Alzheimer's disease).
10. As of 1995, tests for cystic fibrosis, Duchenne/Becker muscular dystrophy, hemophilia, Gaucher's disease, Huntington's disease, Lou Gehrig's disease, Tay Sachs disease, and thalassemia (among others) were available. See McClure, supra note 1, at 232-33. As of 1996, tests for the presence of the BRCA1 mutation, which predisposes a person to breast or ovarian cancer, were commercially apaglable, and tests to determine the predisposition to Alzheimer's were being developed. See PEOPLE'S MED. SOC'Y, INC., GENETIC TESTING: THE CONTROVERSIAL BACKGROUND CHECK 16 (1997).
11. As of 1995, tests for cystic fibrosis, Duchenne/Becker muscular dystrophy, hemophilia, Gaucher's disease, Huntington's disease, Lou Gehrig's disease, Tay Sachs disease, and thalassemia (among others) were available. See McClure, supra note 1, at 232-33. As of 1996, tests for the presence of the BRCA1 mutation, which predisposes a person to breast or ovarian cancer, were commercially available, and tests to determine the predisposition to Alzheimer's were being developed. See PEOPLE'S MED. SOC'Y, INC., GENETIC TESTING: THE CONTROVERSIAL BACKGROUND CHECK 16 (1997).
12. Cystic fibrosis tests, which cost around $400 in 1993, cost around $125-$150 in 1995, and cost even less in 1997. (The Michigan State University Genetics Clinic quoted a price of $52 for a cystic fibrosis carrier screening test.) If this trend continues, it is predicted that these tests will cost five to ten dollars. See Alfred G. Haggerty, Genetic Advances Are Seen As Boon for Insurers, NAT'L UNDERWRITERS, Mar. 15, 1993, at 25, 25 (Life & Health-Financial Services ed.).
13. Many articles have been published dealing with this subject. For a comprehensive examination, see Eric Mills Holmes, Solving the Insurance/Genetic Fair/Unfair Discrimination Dilemma in Light of the Human Genome Project, 85 KY. L.J. 503 (1997).
14. See id. at 531-78.
15. See infra text accompanying notes 87-93.
16. See infra text accompanying notes 90-91.
17. Although many consumers side with insurers with regard to this issue, the insurers' opposition will be referred to as "consumers" for purposes of objectivity.
18. See generally Carol Lee, Comment, Creating a Genetic Underclass: The Potential for Genetic Discrimination by the Health Insurance Industry, 13 PACE L. REV. 189 (1993) (addressing the potential for abuse of genetic testing by both insurers and private citizens).
19. See Holmes, supra note 8, at 629-44.
20. See infra text accompanying notes 123-34.
21. See Holmes, supra note 8, at 629-44.
22. See infra text accompanying note 135.
23. The McCarran-Ferguson Act, which passed on March 9, 1945, declared that it was in the public's interest for states to regulate the insurance industry, and therefore gave the states that power. 15 U.S.C. §§ 1011-1012 (1994).
24. DNA is a "vast chemical information database" which holds the instructions for making all the products (proteins) a cell will need to carry on bodily functions. Genes within the DNA instruct a particular protein to be produced. NATIONAL CANCER INST., supra note 1, at 1-2.
25. James Watson and Francis Crick were credited with developing the model for the double helix structure in 1953. See RICHARD V. KOWLES, GENETICS, SOCIETY, & DECISIONS 22 (1985).
26. See NATIONAL CANCER INST., supra note 1, at 2, 25, 30.
27. See id. at 2, 30.
28. See id. at 2. "Proteins are the molecules responsible for catalyzing most intracellular chemical reactions (enzymes), for regulating gene expression (regulatory proteins), and for determining many features of the structures of cells, tissues, and viruses (structural proteins). " LEON A. SNYDER ET AL., GENERAL GENETICS 307 (1985) (parentheticals in original).
29. See id. at 2. "Proteins are the molecules responsible for catalyzing most intracellular chemical reactions (enzymes), for regulating gene expression (regulatory proteins), and for determining many features of the structures of cells, tissues, and viruses (structural proteins). " LEON A. SNYDER ET AL., GENERAL GENETICS 307 (1985) (parentheticals in original).
30. See NATIONAL CANCER INST., supra note 1, at 3.
31. Mutations are mistakes in the DNA information sequence. See SNYDER ET AL., supra note 23, at 353-54. "Mutations are abrupt, heritable changes in single genes or small regions of a chromosome." Id. at 353.
32. See NATIONAL CANCER INST., supra note 1, at 4.
33. See id. at 5; see also KOWLES, supra note 20, at 84 (describing how the nucleotide sequence of a gene can be altered); SNYDER ET AL., supra note 23, at 353-89 (providing a more in-depth analysis of gene mutations).
34. See id. at 5; see also KOWLES, supra note 20, at 84 (describing how the nucleotide sequence of a gene can be altered); SNYDER ET AL., supra note 23, at 353-89 (providing a more in-depth analysis of gene mutations).
35. See id. at 5; see also KOWLES, supra note 20, at 84 (describing how the nucleotide sequence of a gene can be altered); SNYDER ET AL., supra note 23, at 353-89 (providing a more in-depth analysis of gene mutations).
36. See NATIONAL CANCER INST., supra note 1, at 5; see also KOWLES, supra note 20, at 217- 18 (suggesting the "nature versus nurture" approach to a person's genotype (actual genetic makeup) and their phenotype (physical expression of their genetic makeup, or genotype)). Kowles instructs that a person's genome (nature) reflects his "potential phenotype." Id. at 218 (emphasis in original). However, environmental factors (nurture) can influence the degree to which the phenotype expresses itself. See id.
37. See NATIONAL CANCER INST., supra note 1, at 5; see also KOWLES, supra note 20, at 217-18 (suggesting the "nature versus nurture" approach to a person's genotype (actual genetic makeup) and their phenotype (physical expression of their genetic makeup, or genotype)). Kowles instructs that a person's genome (nature) reflects his "potential phenotype." Id. at 218 (emphasis in original). However, environmental factors (nurture) can influence the degree to which the phenotype expresses itself. See id.
38. See NATIONAL CANCER INST., supra note 1, at 5.
39. See id.
40. See id.
41. Donald C. Chambers, Genetic Testing and Insurance in the United States, MED. RESOURCE (Lincoln Nat'l Reinsurance, Fort Wayne, Ind.), Oct. 1994, at 3; see also SNYDER ET AL., supra note 23, at 566 ("Quantitative traits are often referred to as multifactorial traits in order to emphasize the many genetic and environmental factors in their determination.") (emphasis in original).
42. Donald C. Chambers, Genetic Testing and Insurance in the United States, MED. RESOURCE (Lincoln Nat'l Reinsurance, Fort Wayne, Ind.), Oct. 1994, at 3; see also SNYDER ET AL., supra note 23, at 566 ("Quantitative traits are often referred to as multifactorial traits in order to emphasize the many genetic and environmental factors in their determination.") (emphasis in original).
43. See KOWLES, supra note 20, at 233 (discussing oncogenes - genes which may cause cancer if activated by, among other things, environmental factors).
44. Parents pass on a particular copy of a gene to their offspring. As stated supra note 1, each parent donates a haploid number of chromosomes to the offspring, giving it a diploid number. In donating a haploid number of chromosomes, each parent donates one allele to the offspring. See Brian R. Gin, Genetic Discrimination: Huntington's Disease and the Americans with Disabilities Act, 97 COLUM. L. REV. 1406, 1414 & n.45 (1997). The combination of the two alleles forms the particular gene. See id. Huntington's disease only requires the presence of one allele in order for the disease to manifest itself. (The dominant allele must be present in the pair for manifestation of Huntington's.) See id. Suppose the dominant Huntington's allele will be represented by "H," and the recessive allele (which does not cause Huntington's), will be represented by "h." If each parent donates h alleles, the offspring is considered homozygous recessive (hh) for Huntington's and the disease will not manifest itself. See id. However, if one parent donates an H allele, and the other parent donates an h allele, the offspring is considered heterozygous dominant (Hh) for Huntington's and the disease will manifest itself, since the dominant allele, H, is present. See id. Cystic fibrosis occurs in the presence of a homozygous recessive pair of alleles. See Janet A. Kobrin, Confidentiality of Genetic Information, 30 UCLA L. REV. 1283, 1289 & n.38 (1983). Suppose the dominant allele for cystic fibrosis is "C," and the recessive allele is "c." If each parent donates C alleles, a homozygous dominant pairing occurs (CC), and the disease does not manifest itself. See id. If one parent donates a C allele, and the other parent donates a c allele, a heterozygous dominant condition occurs (Cc), and the disease does not manifest. See id. However, if each parent donates c alleles, a homozygous recessive condition occurs (cc), and the disease manifests itself. See id. Many different diseases require different pairings of alleles in order to manifest. Some require a homozygous dominant allele pair and some require a heterozygous dominant allele pair. See id.; see also FRISTROM & SPIETH, supra note 1, at 156-57; KOWLES, supra note 20, at 40-44; SNYDER ET AL., supra note 23, at 8.
45. Parents pass on a particular copy of a gene to their offspring. As stated supra note 1, each parent donates a haploid number of chromosomes to the offspring, giving it a diploid number. In donating a haploid number of chromosomes, each parent donates one allele to the offspring. See Brian R. Gin, Genetic Discrimination: Huntington's Disease and the Americans with Disabilities Act, 97 COLUM. L. REV. 1406, 1414 & n.45 (1997). The combination of the two alleles forms the particular gene. See id. Huntington's disease only requires the presence of one allele in order for the disease to manifest itself. (The dominant allele must be present in the pair for manifestation of Huntington's.) See id. Suppose the dominant Huntington's allele will be represented by "H," and the recessive allele (which does not cause Huntington's), will be represented by "h." If each parent donates h alleles, the offspring is considered homozygous recessive (hh) for Huntington's and the disease will not manifest itself. See id. However, if one parent donates an H allele, and the other parent donates an h allele, the offspring is considered heterozygous dominant (Hh) for Huntington's and the disease will manifest itself, since the dominant allele, H, is present. See id. Cystic fibrosis occurs in the presence of a homozygous recessive pair of alleles. See Janet A. Kobrin, Confidentiality of Genetic Information, 30 UCLA L. REV. 1283, 1289 & n.38 (1983). Suppose the dominant allele for cystic fibrosis is "C," and the recessive allele is "c." If each parent donates C alleles, a homozygous dominant pairing occurs (CC), and the disease does not manifest itself. See id. If one parent donates a C allele, and the other parent donates a c allele, a heterozygous dominant condition occurs (Cc), and the disease does not manifest. See id. However, if each parent donates c alleles, a homozygous recessive condition occurs (cc), and the disease manifests itself. See id. Many different diseases require different pairings of alleles in order to manifest. Some require a homozygous dominant allele pair and some require a heterozygous dominant allele pair. See id.; see also FRISTROM & SPIETH, supra note 1, at 156-57; KOWLES, supra note 20, at 40-44; SNYDER ET AL., supra note 23, at 8.
46. Parents pass on a particular copy of a gene to their offspring. As stated supra note 1, each parent donates a haploid number of chromosomes to the offspring, giving it a diploid number. In donating a haploid number of chromosomes, each parent donates one allele to the offspring. See Brian R. Gin, Genetic Discrimination: Huntington's Disease and the Americans with Disabilities Act, 97 COLUM. L. REV. 1406, 1414 & n.45 (1997). The combination of the two alleles forms the particular gene. See id. Huntington's disease only requires the presence of one allele in order for the disease to manifest itself. (The dominant allele must be present in the pair for manifestation of Huntington's.) See id. Suppose the dominant Huntington's allele will be represented by "H," and the recessive allele (which does not cause Huntington's), will be represented by "h." If each parent donates h alleles, the offspring is considered homozygous recessive (hh) for Huntington's and the disease will not manifest itself. See id. However, if one parent donates an H allele, and the other parent donates an h allele, the offspring is considered heterozygous dominant (Hh) for Huntington's and the disease will manifest itself, since the dominant allele, H, is present. See id. Cystic fibrosis occurs in the presence of a homozygous recessive pair of alleles. See Janet A. Kobrin, Confidentiality of Genetic Information, 30 UCLA L. REV. 1283, 1289 & n.38 (1983). Suppose the dominant allele for cystic fibrosis is "C," and the recessive allele is "c." If each parent donates C alleles, a homozygous dominant pairing occurs (CC), and the disease does not manifest itself. See id. If one parent donates a C allele, and the other parent donates a c allele, a heterozygous dominant condition occurs (Cc), and the disease does not manifest. See id. However, if each parent donates c alleles, a homozygous recessive condition occurs (cc), and the disease manifests itself. See id. Many different diseases require different pairings of alleles in order to manifest. Some require a homozygous dominant allele pair and some require a heterozygous dominant allele pair. See id.; see also FRISTROM & SPIETH, supra note 1, at 156-57; KOWLES, supra note 20, at 40-44; SNYDER ET AL., supra note 23, at 8.
47. Parents pass on a particular copy of a gene to their offspring. As stated supra note 1, each parent donates a haploid number of chromosomes to the offspring, giving it a diploid number. In donating a haploid number of chromosomes, each parent donates one allele to the offspring. See Brian R. Gin, Genetic Discrimination: Huntington's Disease and the Americans with Disabilities Act, 97 COLUM. L. REV. 1406, 1414 & n.45 (1997). The combination of the two alleles forms the particular gene. See id. Huntington's disease only requires the presence of one allele in order for the disease to manifest itself. (The dominant allele must be present in the pair for manifestation of Huntington's.) See id. Suppose the dominant Huntington's allele will be represented by "H," and the recessive allele (which does not cause Huntington's), will be represented by "h." If each parent donates h alleles, the offspring is considered homozygous recessive (hh) for Huntington's and the disease will not manifest itself. See id. However, if one parent donates an H allele, and the other parent donates an h allele, the offspring is considered heterozygous dominant (Hh) for Huntington's and the disease will manifest itself, since the dominant allele, H, is present. See id. Cystic fibrosis occurs in the presence of a homozygous recessive pair of alleles. See Janet A. Kobrin, Confidentiality of Genetic Information, 30 UCLA L. REV. 1283, 1289 & n.38 (1983). Suppose the dominant allele for cystic fibrosis is "C," and the recessive allele is "c." If each parent donates C alleles, a homozygous dominant pairing occurs (CC), and the disease does not manifest itself. See id. If one parent donates a C allele, and the other parent donates a c allele, a heterozygous dominant condition occurs (Cc), and the disease does not manifest. See id. However, if each parent donates c alleles, a homozygous recessive condition occurs (cc), and the disease manifests itself. See id. Many different diseases require different pairings of alleles in order to manifest. Some require a homozygous dominant allele pair and some require a heterozygous dominant allele pair. See id.; see also FRISTROM & SPIETH, supra note 1, at 156-57; KOWLES, supra note 20, at 40-44; SNYDER ET AL., supra note 23, at 8.
48. Parents pass on a particular copy of a gene to their offspring. As stated supra note 1, each parent donates a haploid number of chromosomes to the offspring, giving it a diploid number. In donating a haploid number of chromosomes, each parent donates one allele to the offspring. See Brian R. Gin, Genetic Discrimination: Huntington's Disease and the Americans with Disabilities Act, 97 COLUM. L. REV. 1406, 1414 & n.45 (1997). The combination of the two alleles forms the particular gene. See id. Huntington's disease only requires the presence of one allele in order for the disease to manifest itself. (The dominant allele must be present in the pair for manifestation of Huntington's.) See id. Suppose the dominant Huntington's allele will be represented by "H," and the recessive allele (which does not cause Huntington's), will be represented by "h." If each parent donates h alleles, the offspring is considered homozygous recessive (hh) for Huntington's and the disease will not manifest itself. See id. However, if one parent donates an H allele, and the other parent donates an h allele, the offspring is considered heterozygous dominant (Hh) for Huntington's and the disease will manifest itself, since the dominant allele, H, is present. See id. Cystic fibrosis occurs in the presence of a homozygous recessive pair of alleles. See Janet A. Kobrin, Confidentiality of Genetic Information, 30 UCLA L. REV. 1283, 1289 & n.38 (1983). Suppose the dominant allele for cystic fibrosis is "C," and the recessive allele is "c." If each parent donates C alleles, a homozygous dominant pairing occurs (CC), and the disease does not manifest itself. See id. If one parent donates a C allele, and the other parent donates a c allele, a heterozygous dominant condition occurs (Cc), and the disease does not manifest. See id. However, if each parent donates c alleles, a homozygous recessive condition occurs (cc), and the disease manifests itself. See id. Many different diseases require different pairings of alleles in order to manifest. Some require a homozygous dominant allele pair and some require a heterozygous dominant allele pair. See id.; see also FRISTROM & SPIETH, supra note 1, at 156-57; KOWLES, supra note 20, at 40-44; SNYDER ET AL., supra note 23, at 8.
49. See Don Chambers, 'Predisposed' vs. 'Presymptomatic': There's a Big Difference, MED. RESOURCE (Lincoln Nat'l Reinsurance, Fort Wayne, Ind.), Jan.-Feb 1995, at 4.
50. Mark A. Rothstein, Genetic Discrimination in Employment and the Americans with Disabilities Act, 29 HOUS. L. REV. 23, 46 (1992) (quoting Letter from Ronnie Blumenthal, Acting Director of Communications and Legislative Affairs, EEOC, to Rep. Bob Wise, Chairman, House Subcommittee on Government Information, Justice and Agriculture (Nov. 22, 1991)).
51. See KOWLES, supra note 20, at 380 (discussing alcoholism and heredity).
52. Predisposed genetic conditions may be multifactorial or single-gene. While a predisposition to heart disease, lung cancer, and alcoholism may require the presence of environmental factors for manifestation, a predisposition to some breast cancers, requiring the presence of the BRCA1 gene, does not require environmental factors in order for the gene to manifest itself. See Marne E. Brom, Insurers and Genetic Testing: Shopping for That Perfect Pair of Genes, 40 DRAKE L. REV. 121, 123-24 (1991).
53. See Steel, supra note 4, at 1506 (providing a table of probabilities of developing breast or ovarian cancer in the presence of the BRCA1 mutation).
54. See Chambers, supra note 35, at 4.
55. See id.
56. See PEOPLE'S MED. SOC'Y, INC., supra note 6, at 1.
57. There have been no described cases of incomplete penetrance with Huntington's disease. See Hayden & Kremer, supra note 3, at 2207.
58. See NORMAN V. ROTHWELL, UNDERSTANDING GENETICS: A MOLECULAR APPROACH 63 (1993).
59. See id.
60. Some patients have developed symptoms for Huntington's in their 80s and 90s. See Hayden & Kremer, supra note 3, at 2203.
61. See ROTHWELL, supra note 44, at 63.
62. See id.
63. See NATIONAL CANCER INST., supra note 1, at 5.
64. See What You Need to Know Before Considering Genetic Testing for Heritable Breast Cancer, THE NETWORK NEWS (National Women's Health Network), Nov. 21, 1996, at 3; see also Steel, supra note 4, at 1506.
65. See What You Need to Know Before Considering Genetic Testing for Heritable Breast Cancer, THE NETWORK NEWS (National Women's Health Network), Nov. 21, 1996, at 3; see also Steel, supra note 4, at 1506.
66. See NATIONAL CANCER INST., supra note 1, at 5; see also KOWLES, supra note 20, at 232- 33.
67. See NATIONAL CANCER INST., supra note 1, at 5; see also KOWLES, supra note 20, at 232-33.
68. See NATIONAL CANCER INST., supra note 1, at 9, 11-12.
69. See id. at 8.
70. See id.
71. See id.
72. See FRISTROM & SPIETH, supra note 1, at 156-57; see also KOWLES, supra note 20, at 4; SNYDER ET AL., supra note 23, at 8; supra note 34.
73. See FRISTROM & SPIETH, supra note 1, at 156-57; see also KOWLES, supra note 20, at 4; SNYDER ET AL., supra note 23, at 8; supra note 34.
74. See FRISTROM & SPIETH, supra note 1, at 156-57; see also KOWLES, supra note 20, at 4; SNYDER ET AL., supra note 23, at 8; supra note 34.
75. See Chambers, supra note 35, at 4; see also supra note 34 (discussing the required allele pairings for different diseases).
76. See NATIONAL CANCER INST., supra note 1, at 9.
77. See id.
78. These tests are known as predictive gene tests. See id. at 11.
79. See McClure, supra note 1, at 232-33.
80. See id.
81. See Haggerty, supra note 7, at 25.
82. 15 U.S.C. §§ 1011-1012 (1994).
83. United States Dep't of Treasury v. Fabe, 508 U.S. 491, 507 (1993) (quoting 15 U.S.C. § 1012(b) (1994)) (emphasis added).
84. Holmes, supra note 8, at 584.
85. Health insurance is generally defined as "insurance providing indemnification for losses caused by illness." 1 LEE R. RUSS & THOMAS F. SEGALLA, COUCH ON INSURANCE § 1:46 (3d ed. 1995).
86. See id. § 1:2.
87. See id. § 1:39.
88. See GENETIC TESTING WORKING GROUP, NATIONAL ASS'N INS. COMM'RS, REPORT OF THE GENETIC TESTING WORKING GROUP TO THE LIFE INSURANCE COMMITTEE 6-7 (1996) [hereinafter NAIC].
89. See id. at 6.
90. See Richard A. Bornstein, Genetic Discrimination, Insurability and Legislation: A Closing of the Legal Loopholes, 4 J.L. & POL'Y 551, 576-77 (1996).
91. A life insurance policy "may, in the absence of contrary legislation or contract provision, be delivered and transferred as other personal property." RUSS & SEGALLA, supra note 67, § 1:39.
92. See NAIC, supra note 70, at 8.
93. 15 U.S.C. §§ 1011-1012 (1994).
94. See RUSS & SEGALLA, supra note 67, § 1:2.
95. An insurer agrees to assume the risk of an applicant individually, or as a member in a group of employees, in exchange for consideration from the individual. This consideration is known as a premium, and may fluctuate based on that individual's personal level of risk, or on the risk within the insured group. See id. § 69:1.
96. Insurance underwriters divide applicants into various risk groups to determine the possibility and degree of loss that the groups might cause the insurers. Risk classification helps to clarify the rates insurers require to protect themselves from excessive losses and ensures that each applicant pays a premium relative to the risk he projects. See MICHAEL C. THOMSETT, INSURANCE DICTIONARY 186 (1989).
97. A person given a standard rating means that he is to be insured at the average rate. A person given a substandard rating means that he is not qualified for standard policy rates. This will lead the insurer to issue a higher premium, or deny the applicant altogether. See id. at 199, 201.
98. See id.
99. See ROBERT J. GIBBONS ET AL., INSURANCE PERSPECTIVES 69 (1992).
100. 15 U.S.C. §§ 1011-1012 (1994).
101. See RUSS & SEGALLA, supra note 67, § 69:38. "The basic principle underlying statutes governing underwriting practices is that insurers have the right to classify risks and to elect not to insure risks if the discrimination is fair." Life Ins. Ass'n v. Commissioner of Ins., 530 N.E.2d 168, 171 (Mass. 1988).
102. 574 N.E.2d 359 (Mass. 1991).
103. Id. at 361-62.
104. See id. at 362.
105. The element of risk is not present when a party has knowledge of their medical future. See RUSS & SEGALLA, supra note 67, § 101:2.
106. "Of those who claim to be nonsmokers and thus stand to gain significantly in terms of lower rates for their insurance, at least six percent of those who say 'I am a nonsmoker' are in fact smokers." Interview with Donald C. Chambers, M.D., Senior Vice President and Chief Medical Director, Lincoln National Corporation, in Fort Wayne, Ind. (June 9, 1997) [hereinafter Chambers Interview]. Dr. Chambers alluded to a test which measures the level of a metabolic byproduct of cigarette nicotine in urine. See id. 89. See GIBBONS ET AL., supra note 81, at 69.
107. See id.
108. See id.
109. The MIB collects health-related information on those applying for health and life insurance. After receiving an application from an individual, the insurer may request information from MIB, to find any health conditions which were unreported by the applicant. See THOMSETT, supra note 78, at 127.
110. Robert J. Pokorski, Genetic Information and Risk Classification and Antiselection, 26 J. INS. MED. 413, 417 (1994-95) (quoting F. Nardi, The Formation of Modern MIB, in 1 ACADEMY OF LIFE UNDERWRITING 13-1 to 13-7 (1984)).
111. See GIBBONS ET AL., supra note 81, at 69.
112. See RUSS & SEGALLA, supra note 67, § 1:2.
113. See McClure, supra note 1, at 237.
114. See id.
115. See id.
116. See id.
117. See NATIONAL CANCER INST., supra note 1, at 10-11.
118. See id. at 9-16.
119. See id. at 14.
120. See RUTH HUBBARD & ELIJAH WALD, EXPLODING THE GENE MYTH 141-42 (1993).
121. See Karen Ann Jensen, Genetic Privacy in Washington State: Policy Considerations and a Model Genetic Privacy Act, 21 SEATTLE U. L. REV. 357, 364-65 (1997).
122. See INSTITUTE OF MED., ASSESSING GENETIC RISKS 248 (Lori B. Andrews et al. eds., 1994).
123. See id. at 249.
124. Suzanne E. Stipe, Genetic Testing Battle Pits Insurers Against Consumers, BEST'S REV.: LIFE/HEALTH INS., Aug. 1996, at 38, 43 (citing comments by New Jersey Assembly Democratic Leader Joseph V. Doria concerning the passage of a New Jersey genetic testing bill which he sponsored).
125. See Lisa N. Geller et al., Individual, Family, and Societal Dimensions of Genetic Discrimination: A Case Study Analysis, 2 SCI. & ENGINEERING ETHICS 71 (1996).
126. See id. at 76.
127. See KOWLES, supra note 20, at 151-52.
128. See Geller et al., supra note 108, at 76.
129. See Donald C. Chambers, Genetic Discrimination: Much Press, Little Substance, MED. RESOURCE (Lincoln Nat'l Reinsurance, Fort Wayne, Ind.), Jan./Feb. 1997, at 3, 3.
130. See Geller et al., supra note 108, at 79.
131. See id.
132. Hemachromatosis is a genetic disorder where iron accumulates in tissues, leading to heart and liver damage. Regular phlebotomies (withdrawals of blood) are performed in order to keep the iron level down and to prevent organ damage. See More Screening Needed for Hemachromatosis, GENESIS REP.-DX (Genesis Group Ass'n), Jan. 1, 1996, available in 1996 WL 9660649.
133. See Chambers Interview, supra note 88.
134. See Dorthy Nelkin & Lori Andrews, Do the Dead Have Interests? Policy Issues for Research After Life, 24 Am. J.L. & Med. 261, 268 (1998).
135. See Chambers Interview, supra note 88.
136. 644 A.2d 295 (R.I. 1994).
137. Id. at 306 (Lederberg, J. dissenting).
138. 676 A.2d 1347 (R.I. 1996).
139. Id. at 1356.
140. Holmes, supra note 8, at 578.
141. Id.
142. 15 U.S.C. § 1012(b) (1994); see also American Deposit Corp. v. Schacht, 84 F.3d 834, 838 (7th Cir. 1996).
143. 15 U.S.C. § 1012(b) (1994); see also American Deposit Corp. v. Schacht, 84 F.3d 834, 838 (7th Cir. 1996).
144. See Holmes, supra note 8, at 629-44, for a list of the various state legislation regulating insurers' access to genetic information.
145. See Bornstein, supra note 72, at 579-88, for a list of proposed federal legislation concerning insurers' access to genetic information.
146. Pub. L. No. 104-191, 110 Stat. 1936 (codified as amended in scattered sections of 26, 29 & 42 U.S.C.).
147. See id. § 101 (amending 29 U.S.C. § 1181(b)(1)(B)).
148. See Genetic Information Nondiscrimination in Health Insurance Act of 1997, S. 89, 105th Cong. (1997).
149. See Genetic Information Nondiscrimination in Health Insurance Act of 1997, H.R. 306, 105th Cong. (1997).
150. S. 89 § 713(a)(1),(2).
151. 42 U.S.C.A. §§ 12101-12213 (1995 & West Supp. 1998).
152. 29 U.S.C.A. §§ 1001-1461 (West 1999).
153. See Holmes, supra note 8, at 644-49.
154. Id.
155. See id. at 645.
156. Id. at 647.
157. N.M. Stat. Ann. § 59A-23E-11 (Supp. 1998).
158. Holmes, supra note 8, at 645-46.
159. See id. at 646.
160. See id. at 652-56.
161. See supra text accompanying notes 18, 64-66.
162. See supra text accompanying notes 65-66.
163. DONALD C. CHAMBERS, LINCOLN NAT'L REINSURANCE, RISKY BUSINESS: THE COLLISION OF GENETICS AND THE INSURANCE INDUSTRY 5 (1996).
164. ERNEST GELHORN & RONALD M. LEVIN, ADMINISTRATIVE LAW AND PROCESS IN A NUTSHELL 2 (4th ed. 1997).
165. 147. Id. at 1.
166. Statement by HHS Secretary Donna Shalala, U.S. NEWSWIRE, June 26, 1997, available in 1997 WL 5713774 (emphasis added).
167. See generally NATIONAL CANCER INST., supra note 1.