Thursday, July 12, 2007

They Don't Warn The Public About the Risks of Rising Paternal Age and Now This


By Byron J. Richards, CCN
July 12, 2007
On Wednesday, July11, 2007 the House passed HR.2900 without allowing the Ron Paul (R-TX) amendments to protect dietary supplements. Representatives Frank Pallone, Jr. (D-NJ), John Dingell (D-MI), Henry Waxman (D-CA), and others falsely proclaimed that they were doing America a favor by passing this sweeping FDA-supported legislation that grants the rouge agency more power and money, and even transforms it into a quasi drug company.
Both the House and Senate (S.1082) have made the fatally flawed assumption that the reason for so many deaths and injuries from drugs was due to the FDA’s lack of resources. In reality, it is the INTENTION of FDA management that is the problem, combined with the simple fact that multiple drugs are extremely toxic and don’t work as advertised. Giving the FDA more power and money will only cause the agency to speed more drugs onto the market faster with even less safety testing – while abusing its power and actively stamping out competition to drugs.
FDA management is in bed with Big Pharma and this new legislation makes matters significantly worse through the creation of the Reagan-Udall Foundation for the FDA. This new entity places the FDA in charge of drug design, drug patents, drug licenses, and the creation of new marketing entities/companies. Such a relationship with private industry is an unprecedented conflict of interest, totally at odds with drug safety. The current commissioner of the FDA, Andrew von Eschenbach, M.D. is little more than a Big Biotech sales rep with massive industry connections.
The House, like the Senate, will continue to allow direct to consumer advertising of new drugs with unknown risks – a flagrant safety risk that will cost many people their lives. Congressional leaders said they couldn’t prevent this advertisement for fear of violating the first amendment rights of drug companies. What a joke. The FDA routinely squashes the first amendment rights of American citizens to understand natural health options and the science that explains how they can prevent and treat disease. Thus, the first amendment argument is simply a matter of convenience. The FDA wants to actively suppress information that will help people, yet allow highly risky and misleading promotion of toxic substances often for untested uses. The FDA even wants to prevent citizens from suing drug companies when they are injured, thus protecting Big Pharma. FDA tyranny, based on this type of arbitrary and unrestrained exercise of power, is used to promote and protect the pharmaceutical industry while at the same time undermining the dietary supplement industry.
Both the House and Senate think it is completely fine that the drug industry pay the FDA fees so that the FDA can approve new drugs faster. Indeed, the FDA and Big Pharma met 112 times to work out their partnership before the FDA let Congress know what it wanted to see in HR.2900 and S.1082. This is like paying the mob for protection. A careful look at the history of the FDA shows it is little more than a bully that protects vested interests at the expense of human health. It is a pitiful agency. It is little wonder than the majority of Americans don’t trust the FDA.
Big Pharma owns the FDA and Congress. The drug industry sees FDA management and Congressional leaders as a training pool for future Big Pharma jobs – based on how well Big Pharma is supported. There will certainly be plenty of rewards to pass out after this legislation becomes law.
It is a sick situation that this new fake safety legislation provides the FDA with unprecedented new power to stamp out competition to drug companies as well as expose Americans to far greater safety risks than ever before. Provisions within the legislation that creates the Reagan-Udall Foundation for the FDA will allow the FDA to remove any dietary supplement from the market based on its whim.

It is now only a matter of time and a formality before HR.2900 and S.1082 become law. There will be a little bit of haggling in the conference committee, as Big Pharma will takes its last chance at watering down any meaningful reform (of which there is very little). Big Pharma will whine that this legislation is too tough on them, which is a fallacy. This legislation is the Big Pharma dream come true. In a football analogy the only question is the final score. Will Big Pharma win by 28-7 or will it win by 42-7. Big Pharma has just cleaned the clock of Americans. We should not forget the gutless Congressional puppets that made it happen.

A new tone has been set. A new chart has been plotted. Congress has transformed the FDA into a quasi drug company with unprecedented new regulatory power to control all health options in America. How many deaths and injuries will it take for a comatose and medicinally-overdosed public to wake up?

By Byron J. Richards, CCN

July 12, 2007


Monday, July 09, 2007

Over the last decade, it was shown that the risk for many complex genetic diseases was also correlated with paternal age.

Paternal Age and Schizophrenia An Expert Interview with Dolores Malaspina, M.D., M.P.H.
(Great Neck, NY -

March 23, 2006) — Scientists have linked paternal age to genetic diseases since the 1950s, and some have suggested an association between the age of the father and the risk for schizophrenia. In 2001, Dolores Malaspina, M.D., M.P.H., and her colleagues reported their research identifying a relationship between paternal age and the occurrence of schizophrenia. On behalf of Medscape* Jessica Gould interviewed Dr. Malaspina, Professor of Clinical Psychiatry at Columbia University and Research Psychiatrist at New York State Psychiatric Institute in New York City. Dr. Malaspina elaborates on her research and speaks about new directions in genetic research on schizophrenia. (NARSAD NOTE: Dr. Malaspina was a NARSAD 1993 and 1995 Young Investigator and a 2001 Independent Investigator.)Medscape: Tell me about your research on paternal age and schizophrenia.Dolores Malaspina: I have been compelled by the idea that schizophrenia is not a single disease. The consensus in the field is that schizophrenia is a syndrome, and a syndrome is a collection of different disorders. Yet there is still some controversy over whether or not there are variants of schizophrenia that might have separate causes and respond differently to various medications.Since beginning my research in the late 1980s, I have focused on this heterogeneity, and one way that I've done that is by examining aspects of the disease in people who come from densely affected families, where two or more relatives have schizophrenia, and comparing them with cases of schizophrenia that have no family history of any chronic psychosis.Now, in genetic research, it's known that for human genetic diseases, when a new case presents itself in a family, the mutation almost always arises during spermatogenesis. We have known for almost 100 years that the late born children in a family have more new genetic diseases. In the 1950s, a scientist named Penrose showed that only the age of the father predicts these genetic diseases. Over the last decade, it was shown that the risk for many complex genetic diseases was also correlated with paternal age. I thought that if schizophrenia cases with no family history were due to new genetic events, maybe they would also be correlated with the father's age.

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Sunday, July 08, 2007

Type 1 diabetes risk rises with the age of the father and mother and yet there is no warning for the public

1: Diabet Med. 2005 Feb;22(2):200-6. Links
Parental age at delivery, birth order, birth weight and gestational age are associated with the risk of childhood Type 1 diabetes: a UK regional retrospective cohort study.Cardwell CR, Carson DJ, Patterson CC.
Department of Epidemiology & Public Health, The Queen's University of Belfast, Belfast, UK.

AIMS: To investigate perinatal risk factors for childhood Type 1 diabetes in a UK population cohort. METHODS: Perinatal data have been routinely recorded in Northern Ireland for all births in the period 1971-86 (n = 447 663). Diabetes status at the age of 15 years was ascertained in this cohort by identifying 991 children from 1079 registered with Type 1 diabetes diagnosed from 1971 to 2001 and date of birth in the period 1971-86. RESULTS: Increased Type 1 diabetes risk was associated with higher maternal age, paternal age, birth weight and birth weight for gestational and lower gestational age. After adjustment for maternal age, the association between Type 1 diabetes and paternal age remained significant [relative risk (RR) = 1.52 (1.10, 2.09) comparing father's age 35 years or more to less than 25 years] but not vice versa [RR = 1.11 (0.80, 1.54) comparing mother's age 35 years or more to less than 25 years]. Increased birth order was associated with a significant decrease in the risk of Type 1 diabetes [adjusted RR = 0.75 (0.62, 0.90) comparing birth order three or more with firstborn], but this only became apparent when adjustment was made for maternal age. Furthermore this association with birth order was significant only for diabetes diagnosed under the age of 5 years. CONCLUSIONS: Our analysis demonstrates, for the first time in a UK regional cohort setting, that maternal age and paternal age at delivery, birth order, birth weight and gestational age are significantly associated with Type 1 diabetes risk.

PMID: 15660739 [PubMed - indexed for MEDLINE]

1: Eur J Pediatr. 1999 May;158(5):362-6. Links
Risk factors for type I diabetes mellitus in children in Austria.Rami B, Schneider U, Imhof A, Waldhör T, Schober E.
University Children's Hospital Vienna, Austria.

The aim of this study was to investigate environmental risk factors in the development of type 1 diabetes mellitus in a population-based case-control study. Parents of all patients with manifestation of type 1 diabetes between 1989 and 1994 in Vienna were asked to complete a questionnaire (n = 114). Control children (n = 495), matched for age and sex, were randomly recruited from all schools in Vienna. Fathers of diabetic children were significantly older at the time their children were born than fathers of control children (P = 0.015). Children with diabetes were more likely to be second- or third-born children (P<0.05) and fewer went to kindergarten than the control group children (P = 0.007). No significant difference in duration of gestation, percentage of delivery by caesarean section, birth weight or length was found. Neonatal jaundice was more often observed in the patient group (P = 0.038). Breast feeding was reported by 82.7% of mothers of diabetic children and by 81% of mothers of control children, and the duration of breast feeding was longer in patients than in controls (n.s.). CONCLUSION: In our study, the development of type 1 diabetes mellitus was associated with higher paternal age and neonatal jaundice. No correlation could be found with dietary intake of cow's milk products in early infancy, vaccination and other environmental factors.


Saturday, July 07, 2007

Why Would There Be No Male Biological Clock?

Why are American young sicker than our parents?

Press Releases
2007 Releases
Chronic Conditions in Children Will Pose Future Health and Welfare Challenges
Investigators describe probable causes, forecast impact on health, welfare system

For immediate release: Tuesday, June 26, 2007

Boston - The increased incidence of chronic conditions among American children predicts serious strains on health care and social welfare systems in the future, caution investigators from Massachusetts General Hospital (MGH) and Harvard School of Public Health (HSPH). In a commentary in the June 27 Journal of the American Medical Association - an issue devoted to pediatric chronic disease - the authors explain how rates of obesity, asthma and attention-deficit hyperactivity disorder (ADHD) have increased over the past three decades, review factors that may underlie those increases and examine future implications.

"These new epidemics in chronic health conditions among children and youth will translate into major demands on public health and welfare in upcoming decades," explains James Perrin, MD, of the Center for Child and Adolescent Health Policy, MassGeneral Hospital for Children, one of the authors of the report. "Active prevention efforts likely offer the best hope of reversing these trends."

The authors reviewed data from many sources and numerous studies in scientific journals to document their observation that more children have chronic health conditions today. They found that rates of obesity in children and adolescents have more than tripled - from 5 percent in the 1970s to 18 percent today. The incidence of asthma has more than doubled to almost 9 percent, and the diagnosis of ADHD has also increased in past decades to include about 6 percent of school aged children. Overall, from 15 to 18 percent of children and adolescents have some sort of chronic health condition, nearly half of whom could be considered disabled.

But the study in this week’s Journal of the American Medical Association documents a grim prognosis for the next generation of workers: they are going to be fatter, more asthmatic, and suffering from far more neurological disorders than any previous generation of American young people. And its young people who are most likely to go without health care coverage.

“We’re going to see increased health expenditures for people in their 20s,” said James Perrin, a professor of pediatrics at the Harvard Medical School and lead author of the report. “They’ll be coming to institutions for health care without any means of paying for it.”


Advanced paternal age is associated with an increased risk of new mutations. Fragile X Hemophilia, Duchenne's, autism, schizophrenia

Advanced paternal age is associated with an increased risk of new mutations. All populations are at risk. The relative increased risk for these defects is related to advanced age of the father for autosomal dominant conditions and the maternal grandfather for X-linked conditions. Family histories will not provide clues as these types of mutations are sporadic. Examples of autosomal dominant conditions associated with advanced paternal age include achondroplasia, neurofibromatosis, Marfan syndrome, Treacher Collins syndrome, Waardenberg syndrome, thanatophoric dysplasia, osteogenesis imperfecta, and Apert syndrome Examples of X-linked conditions associated with increased maternal grandfather's age include fragile X, hemophilia A (Factor VIII deficiency), Hemophilia B (Factor IX deficiency), Duchenne muscular dystrophy, incontinentia pigment), Hunter syndrome, Bruton agammaglobulinemia, and retinitis pigmentosa.

1 The FMR-1 gene is located on the X chromosome. This gene is responsible for instructing the cell to make FMRP, a protein assumed to be essential for normal brain functioning.
A Single Gene Disorder
Fragile X Syndrome is a single gene disorder located on the X chromosome. Understanding the basics of fragile X syndrome requires an understanding of how genes themselves are constructed and what they do.
Genes are made up of DNA, which provides the blueprint for life. This blueprint is a code containing four letters (C, G, A, T), abbreviations for four different nucleotides (cytosine, guanine, adenine, and thymine). Nucleotides are the essential building blocks that make DNA. The letters and the sequences in which they are arranged construct the messages that lead the body to produce key proteins.

Fragile X syndrome results from a mutation (a change in the typical DNA sequence) known as trinucleotide repeat expansion. This means that a series of three particular nucleotides (CGG) in the DNA is greatly expanded beyond its normal size, disrupting the normal messages that need to be sent. This fact was discovered in 1991 by several teams of researchers studying the X chromosome.

In the FMR-1 gene located on the X chromosome, most individuals have CGG repeat that occurs between 5 and 50 times, the average being around 30. These individuals are normal with respect to fragile X syndrome, and usually carry no risk of transmitting it, although the 40—60 repeat range is sometimes considered a "gray zone" which may or may not be unstable (have a risk of expanding). Some individuals have CGG sequences that are repeated in the range of about 50 to 200. These individuals are generally referred to as premutation carriers. This means that they carry the syndrome and can transmit it to their children. Premutation carriers, however, are not usually affected by fragile X syndrome. When the number of CGG repeats expands beyond 200, the individual usually has the full mutation. This means that they have fragile X syndrome and will experience the impairments and delays associated with the syndrome.

Detecting Fragile X Syndrome

Fragile X syndrome is detected through a DNA analysis that almost always requires drawing blood. The technique for identifying fragile X syndrome is a specialized process and not all genetic labs have this capability. For those that do have this capability, the procedure is virtually 100 percent reliable. Fragile X can be detected prenatally or in newborns through DNA testing. Also, the carrier status of parents can be accurately determined. However, these tests are not routinely done and must be specifically requested. It is impossible to determine how severely affected the child might be based on this procedure.

Inheriting Fragile X Syndrome

Fragile X syndrome is carried on the X chromosome. Since both males (XY) and females (XX) each have at least one X chromosome, both can be carriers or have the syndrome. If a father is a carrier, he can only pass the gene defect to his daughters, since he transmits a Y chromosome to his sons. All of his daughters will inherit the gene, and as far as is known, transmission from father to daughter only occurs in the premutation state. In other words, if a daughter inherits the gene from her father, she will have the premutation, not the full mutations. Interestingly, this happens even if the father has the full mutation, as the sperm cells of males with the full mutation have been shown to be in the premutation phase.

If a mother is the carrier, she can pass the gene defect to either sons or daughters, since she contributes an X chromosome to each. Children of carrier mothers have a 50 percent chance of inheriting the gene, since the mother has two Xs to give and only one is affected. It is through mothers that the gene can expand from the premutation to the full mutation. So, a carrier mother can have normal children, children with the premutation, or children with the full mutation.

The chances of expansion into the full mutation increase with successive generations. Thus the gene could be passed down in the premutation phase for several generations without anyone suspecting that the family has a genetic disorder that ultimately will lead to mental retardation or other developmental disabilities.

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Friday, July 06, 2007

NW Sperm Bank--Sperm Donor Between 18 and 35 to minimize age related genetic abnormalities

Donor Standards

Our donors are recruited from the Northwest US. Most of our donors are either starting, currently involved with, or have finished their higher education at the time of their participation in our donor program. All donors are between 18 and 35 years of age in order to minimize age related genetic abnormalities. All donors are frozen in very limited quantities in order to guarantee that the number of pregnancies created from any one donor are limited. We stop further sales to new clients at 10 reported successes. Although all donor histories are reviewed to provide you with donors that should give you a great chance of concieving a healthy and normal baby, there is of course no way to guarantee such an outcome. As all donor family histories will present with their own unique positive and negative attributes, we encourage all clients to review donor information thoroughly prior to purchase and use of specimens.

All of our donors are commercial anonymous donors. We do not provide the identity of any of our donors to clients. All of our donors are asked if they are willing to meet with, or be contacted by, legal aged children that could be produced through their donations. If the donor expresses that he is willing to entertain future contact by legal aged children, then the child must approach the Cryobank to initiate the potential donor contact.
Our donor screening meets or exceeds the standards set forth by the FDA, AATB, ASRM. (Food and Drug Administration, American Association of Tissue Banks, American Society for Reproductive Medicine) Our lab has been through FDA inspection in 2007.


Are Most New Copy Number Variations (CNVs) due to increasing Paternal Age and Sperm DNA Mutations?

Madison-based NimbleGen Systems Inc., which is being acquired by Swiss pharmaceutical giant Roche, announced that the Genome Structural Variation Consortium's Copy Number Variation (CNV) Project has selected NimbleGen human CGH microarrays as the platform to conduct Phase 2 of their studies. The project aims to extend the current human genome CNV map down to a 500 bp resolution, which would be a significant improvement over the existing map released last year.


Wednesday, July 04, 2007

Older Age of the Parent Who Donated the Extra X Chromosome is a Risk Factor For Klinefelter's Syndrome

At least one of the X chromosomes must have come from the mother and the Y chromosome must have come from the father. However, the additional X chromosome may originate from either parent. A maternal origin for the extra X is slightly more common2. Older age of the parent who donated the additional chromosome is a risk factor for Kinefelter's syndrome3.
Klinefelter's Syndrome, a sex-linked disorder << back
3 Jul 2007
Paul Hewish, general practitioner and author, Norfolk. Reviewed by Louise Newson, general practitioner, Birmingham
Klinefelter's syndrome is XXY karyotype but there may be variations and mosaics.
Presentation is often not until puberty when they develop gynaecomastia and fail to develop sexually. Testes are small was absent sperm production.
They are tall and thin.
Testosterone therapy will aid sexual maturation, muscle development and prevent fatigue and osteoporosis but there is infertility.
There is increased risk of malignancies including those of testicular origin and breast cancer.
Intelligence is slightly below normal.
Life expectancy is normal....................

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Tuesday, July 03, 2007

Neural Tube Defects Fathers 28.7 plus or minus 5.81 years

Prenat Diagn. 2007 Jun 29; [Epub ahead of print]Neural tube defects in the sample of genetic counselling.Joó JG, Beke A, Papp C, Tóth-Pál E, Csaba A, Szigeti Z, Papp Z.
1st Department of Obstetrics and Gynaecology, Faculty of General Medicine, Semmelweis University, Hungary.

Objective This study was conducted to evaluate the major demographic details, diagnostical and clinical features, as well as the risk of recurrence of cases with the major types of neural tube defects (NTD). We also examined the efficiency of ultrasonography based on autopsy examinations during 26 years.Methods The investigations were made into the sample of 743 NTD diagnosed between 1 January 1976 and 31 December 2002. A computerized database was used to sum up the available information about the individual cases; in addition to surveying the couples' major demographic details, we also had the opportunity to collect detailed information about the history, diagnostics (ultrasound) and outcome of the pregnancies as well as the results of the autopsies during the investigation.Results In the 743 cases of NTD, maternal and paternal median ages turned out to be 23.7 years (+/-5.22 years) and 28.7 years (+/-5.81 years), respectively. The male:female ratio was 0.78. Comparable samples of anencephaly and spina bifida allowed for the conclusion that a positive genetic history was equally often found while a positive obstetrical history was almost twice as common in anencephaly. The sensitivity of the maternal serum-alpha fetoprotein (AFP) screening test is the highest in anencephaly and lowest in encephalocele. While the majority of cases of anencephaly were diagnosed before the 24th gestational week, examples of diagnosing spina bifida and encephalocele at a later time could also be found. Among the associated malformations other than those of the central nervous system special mentioning should be made of fetal pyelectasia, cleft palate as well as diaphragmatic herniation. No pathological karyotypes were found in association with encephalocele or spina bifida, but anencephaly was accompanied with trisomy 21 and trisomy 18 in one case each. Anencephaly was found to have the highest risk of recurrence in both nervous system malformations and malformations other than those of the nervous system. Sonography proved to be the most reliable method in cases of enecephalocele.Conclusion The respective median values of maternal and paternal age show that aetas has no role in the occurrence of NTDs. NTDs are more common among girls. Positive genetic, obstetrical and medical findings are of great importance in the incidence of NTDs. Although reliable to only a limited extent, maternal serum-AFP tests are considered to be useful and necessary in screening NTDs, while sonography is the gold standard method in recognizing these frequent malformations. The knowledge of the eventual associated malformations is mainly important in certain cases of spina bifida, which may also yield a good post-natal prognosis. Our data obtained from the sample of 26 years also confirm that the periconceptional administration of folic acid reduces the incidence and risk of recurrence of NTDs. Copyright (c) 2007 John Wiley & Sons, Ltd.

PMID: 17602445 [PubMed - as supplied by publisher]


Monday, July 02, 2007

Why Does Increasing Paternal Age Lead to More Children With Type 1 Diabetes?

T h e B o s t o n G l o b e M o n d a y , M a y 2 1 , 2 0 0 7

By Catherine Elton

Medical research is undergoing a
sea change in its approach to
linking genes to disease. Instead
of hunting individual mutant
genes — a painstaking, expensive
process — researchers are more
often turning to a bold, computer-
driven technique that allows for fast, cheap scanning
of vast regions of DNA for anomalies that can
make people more susceptible to a disease or even directly
trigger illness. It’s not a diagnostic tool yet, but
so-called ‘‘genome-wide association’’ research has over
the past months produced dramatic results linking
hitherto unexplored patches of genetic terrain with
such common killers as heart disease and diabetes.
‘‘We used to hold a single lamp’’ over a suspicious
gene, said Dr. Francis S. Collins, director of the National
Human Genome Research Institute. ‘‘Now
we’re able to light a whole street and survey the entire
The discoveries are the fruit of two huge projects
completed in this decade, the mapping of the human
genome — which showed just how similar human beings
are, with each of us carrying DNA that is 99.9
percent identical — and, just as significant, the mapping
of human genetic variation, completed in 2005.
The regions of variation, although small relative to
the rest of the genome, carry 10 million snippets of
genetic material that vary from individual to individual.
These sections, known as single nucleotide polymorphisms,
or SNPs (pronounced ‘‘snips’’), cause
such happy traits as green eyes or red hair. But they
also are lairs for disease.
In a discovery announced last month by the Broad
Institute of Harvard and MIT, researchers used SNPs
technology to identify genetic variations linked to the
most common form of diabetes. That was a major advance
in uncovering the genetic origins of disease because
the defects occurred in areas of ‘‘junk DNA’’
long dismissed as meaningless, according to Dr. David
Altshuler, professor of medicine at Harvard and
leader of the Broad research team.
The discoveries were possible only because of a
powerful technique that uses thumbnail-sized ‘‘chips’’
smeared with DNA. Each chip can carry up to half a
million SNPs, allowing researchers to scan huge
swaths of an individual’s DNA in seconds, at small
cost. Scan results, in turn, can be quickly compared
with SNP chips containing genetic material from tens
of thousands of other individuals.
So, by comparing DNA from thousands of people
with heart disease or diabetes, say, with DNA from
healthy individuals, researchers can rapidly discover
genetic variances common to those with the disease
and absent from those with no illness.