"It is very possible that PATERNAL AGE is the major predictor of(non-familial) autism." Harry Fisch, M.D., author "The Male Biological Clock". Sperm DNA mutates and autism, schizophrenia bipolar etc. results. What is the connection with autoimmune disorders? Having Type 1 diabetes, SLE,etc. in the family, also if mother had older father. NW Cryobank will not accept a sperm donor past 35th BD to minimize genetic abnormalities.VACCINATIONS also cause autism.

Saturday, August 30, 2008

Older Dad May Be Hazardous to Your Health

The Fifty Foot Blogger: Caution: Dad may be hazardous to your health


Tuesday, August 26, 2008

Biomedical Ethics: A Multidisciplinary Approach to Moral Issues in ...
Journal of American Medical Association (subscription) - Chicago,IL,USA
His conclusion, however, overlooks the significantly increased risk of developmental abnormalities that arise with increasing paternal age and with IVF. ...
See all stories on this topic

Friday, August 22, 2008

Ron Paul's Rally for the Republic Tickets Still on Sale

Min Sannhet: September 2nd Rally for the Republic in Minniapolis, MN


De novo mutations may explain genetic disorders in which an affected child has a mutation in every cell, but has no family history of the disorder.

Wednesday, August 20, 2008

What is a Mutation?A mutation is a permanent change in the DNA sequence of a gene. Mutations in a gene's DNA sequence can alter the amino acid sequence of the protein encoded by the gene.
How does this happen? Like words in a sentence, the DNA sequence of each gene determines the amino acid sequence for the protein it encodes. The DNA sequence is interpreted in groups of three nucleotide bases, called codons
What is a gene mutation and how do mutations occur?
A gene mutation is a permanent change in the DNA sequence that makes up a gene. Mutations range in size from a single DNA building block (DNA base) to a large segment of a chromosome.
Gene mutations occur in two ways: they can be inherited from a parent or acquired during a person’s lifetime. Mutations that are passed from parent to child are called hereditary mutations or germline mutations (because they are present in the egg and sperm cells, which are also called germ cells). This type of mutation is present throughout a person’s life in virtually every cell in the body.
Mutations that occur only in an egg or sperm cell, or those that occur just after fertilization, are called new (de novo) mutations. De novo mutations may explain genetic disorders in which an affected child has a mutation in every cell, but has no family history of the disorder.
Acquired (or somatic) mutations occur in the DNA of individual cells at some time during a person’s life. These changes can be caused by environmental factors such as ultraviolet radiation from the sun, or can occur if a mistake is made as DNA copies itself during cell division. Acquired mutations in somatic cells (cells other than sperm and egg cells) cannot be passed on to the next generation.
Mutations may also occur in a single cell within an early embryo. As all the cells divide during growth and development, the individual will have some cells with the mutation and some cells without the genetic change. This situation is called mosaicism.
Some genetic changes are very rare; others are common in the population. Genetic changes that occur in more than 1 percent of the population are called polymorphisms. They are common enough to be considered a normal variation in the DNA. Polymorphisms are responsible for many of the normal differences between people such as eye color, hair color, and blood type. Although many polymorphisms have no negative effects on a person’s health, some of these variations may influence the risk of developing certain disorders.. Each codon specifies a single amino acid in a protein.
Posted by Nirjala at 11:45 PM

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Wednesday, August 20, 2008

Human/male genetic biological clock

When parents are over 35 years old, man and woman alike,
the following cases become prevalent:

Up to a third of all cases of schizophrenia are linked to increasing paternal age.
Men 40 and older are nearly six times more likely to have offspring with autism than men under age 30.

Other research shows that the risk of breast and prostate cancer in offspring increases with paternal age.
The chances of parents of babies with achondroplasia is higher
Older fathers can cause genetic conditions in their offspring, such as birth defects, autism and schizophrenia.
Increased chances of an older woman having a baby with Down's syndrome has been well documented.

Posted by Neriz at Thursday, August 21, 2008
Labels: pasalubong, science

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Where does de novo sporadic autism come from?

1: Sao Paulo Med J. 2008 May;126(3):197-201.
The male biological clock is ticking: a review of the literature.Pasqualotto FF, Borges Júnior E, Pasqualotto EB.
Association Institute Sapientiae, Universidade de Caxias do Sul, São Paulo, Brazil.

The term biological clock is usually used by physicians and psychologists to refer to the declining fertility, increasing risk of fetal birth defects and alterations to hormone levels experienced by women as they age. Female fecundity declines slowly after the age of 30 years and more rapidly after 40 and is considered the main limiting factor in treating infertility. However, there are several scientific reports, chapters in books and review articles suggesting that men may also have a biological clock. The aim of our study was to conduct a review of the literature, based on the Medical Literature Analysis and Retrieval System Online (Medline), to evaluate the male biological clock. After adjustments for other factors, the data demonstrate that the likelihood that a fertile couple will take more than 12 months to conceive nearly doubles from 8% when the man is < 25 years old to 15% when he is > 35 years old. Thus, paternal age is a further factor to be taken into account when deciding on the prognosis for infertile couples. Also, increasing male age is associated with a significant decline in fertility (five times longer to achieve pregnancy at the age of 45 years). Patients and their physicians therefore need to understand the effects of the male biological clock on sexual and reproductive health, in that it leads to erectile dysfunction and male infertility, as well as its potential implications for important medical conditions such as diabetes and cardiovascular diseases.

PMID: 18711662 [PubMed - as supplied by publisher]

Related ArticlesPregnancy outcomes after assisted reproductive technology. [J Obstet Gynaecol Can. 2006] The end of fertility: age, fecundity and fecundability in women. [J Biosoc Sci. 1994] [Sterility and infertility: two concepts] [Cah Que Demogr. 1986] Reproductive potential in the older woman. [Fertil Steril. 1986] Infertility and assisted reproduction in Denmark. Epidemiology and psychosocial consequences. [Dan Med Bull. 2006] » See all Related Articles...


Tuesday, August 19, 2008

Though more research is needed, Malaspina says it’s possible that — just like women — the prime time for becoming a dad is one's 20s and early 30s.

His biological clock is ticking, too
Research links advancing age with declining fertility, genetic defects

Dads: Do you feel sidelined?
Guys, after your sperm has done its job, do you feel like you’re no longer needed? How were you treated during or after your partner's pregnancy? Are men forgotten in the modern pursuit of parenthood?
By Joe Mullich
Special to
updated 4:27 a.m. PT, Wed., June. 27, 2007

Men have long been fathering children well into old age. Tony Randall entered daddyhood at age 77. Charlie Chaplin became a proud pop for the last time at age 73. Rod Stewart had his seventh child at 60 — and may still be on a roll.
But while it seems that older men and fatherhood are no odd couple, scientists have begun questioning the assumption that the biological clock is only a concern for women.
Unlike women, who have a marked decline in fertility in their 30s, men’s biological clocks appear to wind down gradually and progressively over the course of their lives. One study, for instance, found that sperm motility — their ability to be strong swimmers capable of reaching and fertilizing an egg — decreased by a steady 0.7 percent per year for men between the ages of 22 and 80.

Sperm counts appear to decline with age, too. But even men with reduced counts still may be able to father children since it takes just one sperm.
Sperm from older men also may be more likely to contribute to health problems in children. Recent studies have linked older fatherhood with increased risks of schizophrenia, autism, Down syndrome and other disorders in children. And in this case, “older” means as young as 40.
“Young people who want to have a family may want to start considering the age of the father as much as the mother,” says Dr. Dolores Malaspina, a fertility researcher and chair of the psychiatry department at New York University School of Medicine.
In 2001, Malaspina published a study showing that the chance of a child developing schizophrenia rose in concert with the father’s age. The risk was one in 141 for children of fathers under 25, and one in 47 for those with fathers 50 and older. Other studies have replicated those results. Researchers estimate as many as one in four cases of schizophrenia may be linked with a father’s age.
In another study, Malaspina linked paternal age with a greater chance of autism-related disorders — more than a fivefold increased risk for kids born to fathers 40 or older, compared with those born to dads younger than 30.
Since 1980, birth rates have increased 40 percent for fathers ages 35 to 49, while births involving men under 30 have declined. And Malaspina theorizes the rise in fathers’ ages may explain some of the upswing in autism diagnoses, though this hasn’t been proven.
DNA defectsThe culprit behind a man’s ticking biological clock may be the so-called “copy error theory.” Imagine that you copied a document on a Xerox machine. And then you made a copy of the copy. And then a copy of the copy of the copy. With each new generation, the risk of blurs and imperfections increases. The same sort of thing happens with sperm. While women are born with all the eggs they’ll ever have, men constantly produce new sperm by replicating the previous generations of sperm, thus increasing the chance of mutation with each duplication.
Last year, Dr. Andrew Wyrobek, a medical biophysicist at Lawrence Berkeley National Laboratories in Berkeley, Calif., published a study that examined the sperm of 97 healthy men. Breaks in sperm DNA strands, called DNA fragmentation, rose steadily from ages 20 to 80. These breaks can cause fertility problems, pregnancy failures and an increase in some genetic diseases. For instance, genetic mutations in the sperm that can cause dwarfism, a disorder that affects bone growth, increase about 2 percent each year.
“Sperm cells, with the DNA tightly compacted in the sperm head, are one of the few cells in the body that don’t have the ability to repair themselves,” Wyrobek points out.

Learn more about the techniques used to help couples conceive a child.
Exactly what this all means is hazy, as even Wyrobek readily acknowledges. Even if sperm levels decline with age, some men can father children into advanced years — an Australian mine worker made headlines in 1992 by becoming a father at 93 years, 10 months. And though the risk of genetic defects might increase with the father’s age, those risks remain relatively small and can vary from person to person.
What’s more, Dr. Rebecca Z. Sokol, president of the Society for Male Reproduction and Urology and a professor of clinical obstetrics and gynecology at the University of Southern California, says the studies linking a father’s age to abnormalities in sperm DNA and genetic defects are based on “very soft, preliminary data.” Some of the studies, she notes, didn’t control for factors such as alcohol use, which may influence the results.
A sperm shape-up planGiven all this, making recommendations is dicey. Dr. Harry Fisch, director of the Male Reproductive Center at Columbia University Medical Center of New York-Presbyterian Hospital and the author of “The Male Biological Clock,” suggests middle-aged men who plan to become fathers should try to get their sperm in top form.
“If you want to run a marathon, you have to get in shape for it,” Fisch says. “In the same way, you have to train to have a baby.”
Mostly, the recommendations involve sound health practices that are beneficial at any age: quit smoking, avoid excess booze and empty calories, and shed extra pounds since obesity is related to male infertility.
Click for related content
Will science render men useless?Commentary: Becoming a dad, even after death
Another tip: avoid hot tubs. Men’s testicles are outside the body in the scrotum to keep the sperm cooler than the core body temperature, and daily exposure to high levels of heat can cause a reversible decrease in sperm quality.
Fisch also advises older, aspiring fathers go in for a physical examination. Doctors can check for conditions such as varicoceles, dilated veins in the scrotum similar to varicose veins in the legs, which can obstruct sperm. Varicoceles, present in about 40 percent of infertile men, can be corrected with outpatient surgery.
Though more research is needed, Malaspina says it’s possible that — just like women — the prime time for becoming a dad is one's 20s and early 30s.
“Men," she says, "your biological clocks are ticking, too.”
Joe Mullich is a freelance writer in Sherman Oaks, Calif., who has written for Health, Men's Health and Salon.

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Parents Requesting Open Vaccine Education

by Barbara Loe Fisher


While Merck has pulled in $1.5B from sales of GARDASIL vaccine worldwide, there are continuing reports that girls are being crippled and dying after getting the HPV vaccine fast tracked and licensed by the FDA in 2006. Although the roll-out of GARDASIL with an unparalleled multi-million dollar mass media advertising blitz has created a profitable market for the drug company that took huge losses from Vioxx injury/death lawsuits, the persistent reports of Guillain Barre Syndrome (GBS) paralysis, arthritis, seizures and sudden loss of consciousness within 24 hours of vaccination continue to haunt the marketing campaign.

1 in 200 have a mitochondrial disorder

In February, when the US government conceded that vaccines had caused an autism-inducing reaction in little Hannah Poling, most experts declared that her underlying condition, a mitochondrial disorder, was exceedingly rare - so rare, in fact, that it had no bearing on other autism cases.
But today, the United Mitochondrial Disease Foundation announced a “landmark research finding” showing that at least one in 200 healthy humans “harbors a pathogenic mitochondrial mutation that potentially causes disease.” The finding was published in the current issue of the American Journal of Human Genetics. “This is earth shattering news,” UMDF Executive Director and CEO Charles A. Mohan, Jr. told me this evening. “Some of my colleagues are calling it ‘revolutionary.’ We have shown that mitochondrial disease is not rare.”
Mitochondria are the little powerhouses found within most cells and are responsible for producing most of the body’s energy. Mitochondria are key for proper neurotransmission and, for obvious reasons, are highly concentrated in cells of the brain and central nervous system.
Up until now, estimates of mitochondrial disease rates have held steady at about 1-in-4000 people. But this study shows that 20 times that number have genetic mutations that could cause mitochondrial disease.
“What this says to me is that many more than 1-in-4,000 people have mitochondrial disease,” Mohan said. “And it tells me that 1-in-200 could develop some type of mitochondria-related disease over the course of their lifetime, depending in part on environmental triggers.”
Mitochondrial disorders are found at “the core of many well known diseases and chronic illnesses, such as Alzheimer’s disease, Parkinson’s disease and autism spectrum disorders,” a statement from the UMDF said today.
Humans have two types of DNA: nuclear, and mitochondrial. The study looked at 10 mutations in mitochondrial DNA that are known to cause disease, and identified them in the cord blood of 1 in 200 newborn children.
The study looked exclusively at classic mitochondrial “disease.” In the classic form, inherited mutations of mitochondrial DNA are passed down through the mother, causing a wide variety of pathologies, including seizures, digestive problems, paralysis, blindness, heart disease, neurodevelopmental disorders and other problems.
The classic form is often quite severe, and sometimes fatal. But it is not rare.
Which brings us to Hannah Poling: She does not have “classic,” maternally inherited mitochondrial disease.
Hannah does share the same single-point mutation in mitochondrial DNA as her mother, Terry. But this mutation is apparently benign (Terry Poling is just fine), is not described in the medical literature, and is not associated with any pathology at all.
Instead, Hannah seems to have had a much milder, even asymptomatic form of mitochondrial “dysfunction” - one that led to reduced cellular energy, but no obvious signs of severe mitochondrial “disease.”
In April, I reported that researchers in Baltimore were studying 30 children at one autism clinic who all had nearly identical markers for mild mitochondrial dysfunction. One of them was Hannah Poling.
All 30 children were developing normally until they encountered some type of immunological stress and began showing signs of regressive autism soon afterwards.
In 28 cases, the doctors said, typical childhood fevers caused the stress, while in the other two cases, including Hannah, vaccines appeared to be the exacerbating factor.
The doctors - who spoke on a CDC conference call that included executives from the health insurance industry — reported that mitochondrial dysfunction was found in autism “in numbers that make it not a rare occurrence.”
Some estimates currently put the rate of mitochondrial dysfunction in ASD at 7-20%, while rates among regressive autism cases could climb much higher than that.
This milder form of mitochondrial disorder, the doctors said, was probably caused by a mutation found in nuclear (as opposed to mitochondrial) DNA, and inherited through the father — rather than through the mother, as in classic mitochondrial disease.
Shockingly, the nuclear DNA mutations that bring risk of dysfunction could be as common as 1-in-400 to 1-in-50 people - though no one knows how many people have developed actual mitochondrial disorders because of it.
+ Read more:

#2: 678 J Med Assoc Thai Vol. 88 No.5 2005 Correspondence to : Puavilai S, Division of Dermatology, Department of Medicine, Ramathibodi Hospital, Mahidol University, Rama VI Rd, Bangkok 10400, Thailand. Phone:
0-22201-1141, 0-2201-1686, Fax: 0-2201-1211

Herpes Zoster, Clinical Course and Associated Diseases: A 5-Year Retrospective Study at Ramathibodi Hospital Sutasinee Tunsuriyawong, MD*, Siripen Puavilai, MD*
* Department of Medicine, Ramathibodi Hospital, Mahidol University
Objective: Herpes zoster was more frequently found in immunocompromised hosts and elderly persons than in general population. The aim of this study is to find out the distributions of skin lesions, treatments, complications of herpes zoster and associated diseases that occur in concomitant with or after herpes zoster infections.

Material and Method: The medical records of the patients diagnosed as herpes zoster between January 1995- December 2000 were reviewed. Only the patients who were followed up regularly at Ramathibodi hospital for at least 3 years after the first diagnosis of herpes zoster were enrolled into the study. Demographic data, distribution of skin lesions, treatments, complications of herpes zoster and associated diseases were recorded.

Results: Three hundred and ninety-nine cases were enrolled in the study. Three hundred and ninety-eight patients (99.7%) had one dermatomal involvement. Sixty-seven patients (16.8%) had postherpetic neuralgia.
Fifty-six patients had associated HIV infection. In 3 years followed up, 17 patients developed HIV infection, 3 patients developed acute leukemia, 2 patients developed mycosis fungoides.

J Med Assoc Thai 2005; 88(5): 678-81
Full text. e-Journal:

Herpes zoster represents reactivation of the latent varicella-zoster virus in the sensory ganglia. The cutaneous eruptions consist of painful vesicles with or without itchiness which tend to follow a unilateral dermatomal distribution. Prodromal pain may often precede the development of visible lesions. The entire course is usually 2-3 weeks in duration. The two most commonly involved areas for herpes zoster are thoracolumbar (T3-L2) and facial dermatomes (first branch of the trigeminal nerve)(1). Anyone who has had varicella may develop herpes zoster. However, it usually develops in persons older than 50 years, and the incidence increases with advancing age. Herpes zoster is more frequently found in immunocompromised individuals and also as an early manifestation of HIV infection. Approximately 10-20% of patients with herpes zoster will experience a recurrence; such recurrence involves the same dermatome in about 50% of these patients(2).
Disseminated herpes zoster is defined as the presence of more than 20 vesicles outside the primary and adjacent dermatomes. Disseminated herpes zoster is uncommon in immunocompetent patients, but 25-50% of immunocompromised patients may develop this complication(3).
Postherpetic neuralgia is the most common complication of herpes zoster. It is defined as the presence of pain after skin lesions have healed, or pain lasting more than 4-6 weeks after disappearance of cutaneous lesions(4). The pain is often severe and debilitating. It occurs in 8-15% of patients(4), but the incidence increases dramatically with age.
The aim of this study was to find out the clinical course of herpes zoster and the associated diseases that occur in concomitant with or after herpes zoster infection.

Material and Method
Data gathering
Using the Ramathibodi Hospital computerized medical record database, the authors compiled a list of patients diagnosed with herpes zoster who attended J Med Assoc Thai Vol. 88 No.5 2005 679 the Department of Medicine, Ramathibodi Hospital over a 5-year period between January 1995 - December 2000. Only the patients with at least 3 years of followup after the first diagnosis of herpes zoster were enrolled into the study. All available charts were reviewed.
The following data were recorded:
1. Demographic data (sex and age)
2. Underlying diseases at the onset of herpes zoster 3. Clinical manifestations (skin lesions, distribution of skin lesions) 4. Complication (postherpetic neuralgia) 5. Associated diseases that occurred within 3 years of the onset of herpes zoster

There were 612 patients diagnosed as herpes zoster from January 1995 to December 2000. Only 399 records can be enrolled into the study. There were 297 males (74%) and 102 females (26%). Age range from 22-81 years (mean + SD = 59 + 7 years).
Three hundred and eighty-two patients (95.7%) experienced one episode of herpes zoster and only 17 (4.3%) patients had a recurrent episode. The duration from the first episode to the second episode ranged from 4 months - 5 years (mean + SD = 2 + 0.4 years).
Three hundred and ninety-eight patients (99.7%) had one dermatomal involvement and only one patient had disseminated herpes zoster. This patient had associated HIV infection.
Information regarding distribution of skin lesions was available in only 178 patients. The most common anatomic segment was the trunk (114 patients: 64%) followed by the face (64 patients; 36%) (Table1). Among this group, 25 patients (39%) had ophthalmic involvement.
Postherpetic neuralgia was found in 67 patients (16.7%). There were 59 patients aged > 60 years and 8 patients aged between 40-60 years. The duration of postherpetic neuralgia ranged from 1-9 months (mean + SD = 2 + 0.3 months). Thirty-eight patients (56.7%) were treated with tricyclic antidepressants (amitriptyline). Twelve patients (17.9%) were treated with gabapentin. Seven patients (10.4%) were treated with tramadol. The recovery time ranged from 2 weeks to 4 months (mean + SD = 3.4 + 2 weeks) after treatment, There was no difference in recovery times between each treatment.
The underlying diseases of the patients were as follows: HIV in 56 patients (14%) dyslipidemia in 22 patients (5.5%) hypertension in 16 patients (4%), diabetes mellitus in 10 patients (2.5%) and breast cancer in 3 patients (0.75%) (Table2).
After a 3-year follow-up, HIV infection was detected in 17 patients (4.2%), other diseases were erythema nodosum in 5 patients, acute leukemia in 3 patients, mycosis fungoides in 2 patients, pyogenic granuloma at the same area of herpetic infection in 1 patient, squamous cell carcinoma on the upper lip in 1 patient and molluscum contagiosum at the lesion in 1 patient (Table 3).
Table 1. Distribution of skin lesions
Anatomic segment No. of patients % of patients Trunk 114 64 Face 64 36 Table 2. Underlying diseases at the onset of herpes zoster Underlying disease No. of patients % of patients HIV 56 14.0 Dyslipidemia 22 5.5 Hypertension 16 4.0 Diabetes mellitus 10 2.5 Breast cancer 3 0.75 Table 3. Associated diseases detected during 3 years after onset of herpes zoster Diseases No. of patients % of patients Duration detected after onset of herpes zoster (months) HIV 17 4.2 1-7 Erythema nodosum 5 1.2 4-24 Acute leukemia 3 0.75 2-7 Mycosis fungoides 2 0.5 8-24 Pyogenic granuloma 1 0.25 6 Squamous cell carcinoma at upper lip 1 0.25 24 Molluscum contagiosum 1 0.25 unknown 680 J Med Assoc Thai Vol. 88 No.5 2005

Herpes zoster is caused by reactivation of latent varicella-zoster virus (VZV), a double stranded DNA virus in the Alphaherpesvirus family, which is also the causative virus of primary varicella(4). After initial infection with clinical manifestation of chickenpox, VZV remains latent in dorsal root or cranial nerve ganglion for life. Declining virus-specific cellmediated immune response, which occurs naturally as a result of aging or by immunosuppressive illness or immunosuppressive drugs increased the risk of herpes zoster(5).
In the present study, which retrospectively gathered information on 399 patients diagnosed as herpes zoster, affirms previously reported information regarding sex, age and distribution of the skin lesions(1,2,5), but extends and adds to those observations.
Specifically, the present study is the first study to find out the associated diseases with herpes zoster at the time of onset of herpes zoster and three years afterwards.
Eye involvement was found in 39% of the patients who had facial lesions so ophthalmologic consultation is recommended in this group.
Postherpetic neuralgia is the most painful manifestation in these patients. Both the incidence and duration of postherpetic neuralgia are directly correlated with the age of the patients. The reported incidence of postherpetic neuralgia range from 8 to 70% and increased with advancing age. In patients over 50 years, 20% of patients continued to report pain six months after the onset of the rash despite treatment with valacyclovia or famcyclovia(6). In the present study, postherpetic neuralgia occurred in 16.8% of the patients, most of the patients were more than 60 years old. This is in agreement with other studies that postherpetic neuralgia mostly occurred in old age(6,7).
Treatment of postherpetic neuralgia is difficult. Clinical trials have shown that opioids, tricyclic antidepressant and gabapentin reduced the severity and duration of postherpetic neuralgia, either as a single agent or in combination(6,7). In the present study the authors found tricyclic antidepressants were most commonly used (56.7%). But there was no difference in terms of recovery among all pain-relieving medications.
In the present study, the authors found that 56 patients (14%) had HIV infection at the time of diagnosis of herpes zoster. Seventeen patients (4.2%) were detected to have HIV during the follow-up periods. There were three possibilities for the detection of HIV in these 17 patients: 1) some of them might really be new cases 2) some might be in the window period 3) the physician did not request for a laboratory investigation for HIV at the time of onset of herpes zoster. Unfortunately, the information in the medical record was inadequate to clarify these possibilities.
From the previous studies herpes zoster affected about 8-11% of patients with AIDS(4,8). HIV patients commonly have cell counts between 200-400 cells/mm3 when they had the first episode of herpes zoster(9-13).
Unfortunatedly, the authors did not have cell count records of the presented patients. The high percentage of HIV patients in the present study points out the importance of HIV screening in all herpes zoster patients, especially those who in the recognized risk group for HIV infection.
Herpes zoster has been reported to be associated with malignancy, especially in elderly persons. The patients who had Hodgkin’s disease, non-Hodgkin’s lymphomas, and leukemia possess a high risk for herpes zoster(14,15). The patients with solid tumors have a lesser risk for herpes zoster, but treated patients with lung, breast or gynecologic cancers of any age are more likely to have herpes zoster than patients with other solid tumors(15). In the present study, herpes zoster occurred in 3 patients who had underlying breast cancer. After a 3 year follow-up of these patients with herpes zoster, three patients developed acute leukemia, two patients developed mycosis fungoides, and one patient developed squamous cell carcinoma, although herpes zoster is not a risk factor for cancer(16,17).
Long term follow up for at least 2 years should be considered in patients with herpes zoster, especially in the older age group.
In conclusion, the incidence of herpes zoster is increasing nowadays. Old age and immunocompromised host are important predisposing factors and herpes zoster is a frequent early manifestation of HIV infection.
1. Chen TM, George S, Woodruff CA, Hsu S. Clinical manifestations of varicella zoster virus infection. Dermatol Clin 2002; 20: 267-82.
2. Straus SE, Ostrove JM, Inchauspe G, Felser JM, Freifeld A, Croen KD, et al. NIH conference. Varicellazoster virus infections. Biology, natural history, treatment and prevention. Ann Intern Med 1988; 108: 221-37.
3. Straus SE, Schmader KE, Oxman MN. Varicella and herpes zoster. In: Freedberg IM, Eisen AZ, Wolff K, J Med Assoc Thai Vol. 88 No.5 2005 681 Austen KF, Goldsmith LA, Katz SI, eds. Fitzpatrick’s dermatology in general medicine. 6th ed. New York: Mc Graw-Hill, 2003: 2070-85.
4. Vafai A, Berger M. Zoster in patients infected with HIV: A review. Am J Med Sci 2001; 321: 372-80.
5. Gnann JW Jr, Whitley RJ. Herpes zoster. N Engl J Med 2002; 347: 340-6.
6. Johnson RW, Dworkin RH. Treatment options in postherpetic neuralgia. Acta Neurol Scand 1999; 173(Suppl): 13-35.
7. Bonezzi C, Dermartini L. Treatment options in postherpetic neuralgia. Acta Neurol Scan 1999; 173(Suppl): 13-35.
8. Colebunders R, Mann JM, Francis H, Bila K, Izaley L, Ilwaya M, et al. Herpes zoster in African patients: a clinical predictor of human immunodeficiency virus infection. J Infect Dis 1988; 157: 314-8.
9. Veenstra J, Krol A, van Pragg RME, Frissen PH, Schellekens PT, Lange JM, et al. Herpes zoster, immunological deterioration and disease progression in HIV-1 infection. AIDS 1995; 9: 1153-8.
10. Alliegro MB, Dorrucci M, Pezzotti P, Rezza G, Sinicco A, Barbanera M, et al. Herpes zoster and progression to AIDS in a cohort of individuals who seroconverted to human immunodeficiency virus. Clin Infect Dis 1996; 23: 990-5.
11. Veenstra J, van pragg RME, Krol A, Wertheim van Dillen PM, Weigel HM, Schellekens PT, et al. Complications of varicella zoster virus reactivation in HIV-infected homosexual men. AIDS 1996; 10: 393-9.
12. Farizo KM, Buehler JW, Chamberland ME, Whyte BM, Froelicher ES, Hopkins SG, et al. Spectrum of disease in persons with human immunodeficiency virus infection in the United States. JAMA 1992; 267: 1798-805.
13. Peronne C, Lazanas M, Leport C, Simon F, Salmon D, Dallot A, et al. Varicella in patients infected with human immunodeficiency virus. Arch Dermatol 1990; 126: 1033-6.
14. Dolin R, Reichman RC, Mazur MH, Whitley RJ. Herpes zoster-varicella infections in immunosuppressed patients. Ann Intern Med 1978; 89: 375-88.
15. Rusthoven JJ, Ahlgren P, Elhakin T, Whitley RJ. Varicells-zoster infection in adult cancer patients. A population study. Arch Intern Med 1988; 148: 1561-6.
16. Ragozzino MW, Melton LJ, Kurland LT, Chu CP, Perry HO. Risk of cancer after herpes zoster: a population-based study. N Engl J Med 1982; 307: 393-7.
17. Schmader K. Herpes zoster in the elderly: issue related to geriatrics. Clin Infect Dis 1999; 28: 736-9.


Saturday, August 16, 2008

Father's advanced age feeds autism risk A repeat post from Simons Foundation

newsFather's advanced age feeds autism risk
Helen Pearson 25 Feb 2008 9:00 AM

Children of fathers aged 40 or older are nearly six times more
likely to have autism.
Are older fathers more likely to have children with autism? A series of epidemiological studies is giving credence to the idea, suggesting that, with age, sperm may accumulate damage that increases risk in the next generation.

Advancing age of the father is known to be a significant risk factor for schizophrenia1. These studies — along with anecdotal suggestions that fathers of autistic children tend to be older than average — prompted Avi Reichenberg of Mount Sinai School of Medicine, New York, to launch one of the first thorough epidemiological investigations into a link between the two.

Reichenberg and his colleagues had access to a vast database of health information collected from more than 132,000 Israeli adolescents who underwent draft board assessment, including psychiatric screening, before entering the army. The researchers were able to identify those who were diagnosed with autism spectrum disorders (ASD), along with the age of their parents.

Children of fathers in their 30s are about 1.6 times more likely to have ASD than children of fathers below age 30, the study found2. Compared with the youngest group, children of fathers aged 40 or older were nearly six times more likely to have ASD. “It was much stronger than we had thought,” Reichenberg says.

Since then, a handful of other epidemiology studies have backed the autism-paternal age connection. In one of these3, a team led by Lisa Croen of Kaiser Permanente Northern California Division of Research in Oakland, California, mined a health database of more than 130,000 births and found that each decade of paternal or maternal age increased risk of autism spectrum disorder by around 30%.

Paternal age “is still a relatively small contributor,” Croen says, “but when you see something that keeps coming up in different populations and study designs you start thinking there must be something to this.”

The link may be real, but researchers have yet to explain what causes it. Perhaps, says Croen, older parents are simply more attuned to the development of their children and therefore more likely to get a diagnosis. “It could be an artifact,” she says. “We don’t have enough data yet to really rule that out.”

Genetic origins
Another simple explanation is that fathers who themselves have autism or mild social deficits are likely to marry and have children at a later age than other men, and these children inherit factors putting them at high risk of developing the condition themselves.

But Reichenberg says that in his studies he has found no link between traits such as shyness, sensitivity and aloofness in parents and the age at which they have children. “It’s not definitive but the evidence is definitely against such an explanation,” he says.

Many researchers instead favor a genetic origin for the phenomenon. Male germ cells go through multiple rounds of division to manufacture sperm throughout a man’s life and, according to one idea, they may accumulate DNA damage as the molecule is copied again and again.

Sperm produced by older men are more likely to carry genetic defects, and these defects could boost their children’s risk of autism. Female germ cells divide far fewer times.

It is also possible that older sperm are more likely to acquire epigenetic defects: ones that do not change the DNA sequence itself, but that alter the activity of genes due to structural or chemical changes to DNA such as methylation.

These genetic changes arise in the egg or sperm rather than being inherited from the parents. Both concepts fit with the knowledge that the majority of ASD cases have a genetic cause, even though they are also the first in a family.

For precedent, geneticists point to a condition called achondroplasia, a common cause of dwarfism and the textbook example of a genetic condition associated with paternal age. The risk of sperm carrying a single point mutation in the gene for a growth factor receptor is thought to increase with the age of the father.

“It would be overwhelmingly logical,” for something similar to be going on in some cases of autism, says human geneticist Arthur Beaudet at Baylor College of Medicine in Houston, Texas. Perhaps just one or two of the many genes associated with the disorder are susceptible to detrimental point mutations as the germ cells age.

Beaudet says he would like to see genetic and epigenetic analyses of single sperm to see if mutation rates differ in the fathers of autistic children, and between younger and older men. “That would be the approach I’d be enthusiastic about,” he says. Reichenberg says that he is pursuing such studies.

Because there are few clearly defined genes for autism risk, it’s not yet clear where to look for these increased mutation rates. And genome-wide studies looking for differences in the rates of point mutations in many sperm are still too expensive and laborious.

Copy numbers
Last year, molecular studies showed that mutations called copy number variations (CNVs) — genomic chunks that can be deleted or duplicated from one person to the next — appear to be major contributors to sporadic autism.

A group led by Michael Wigler and Jonathan Sebat at the Cold Spring Harbor Laboratory in New York looked for CNVs that were present in autistic individuals, but not in their parents. They found CNVs in 10% of children with sporadic autism, 2% of those with familial autism and 1% of controls4.

This suggests that many more cases of sporadic autism may be attributable to spontaneous mutations — either CNVs or more subtle mutations — than had been realized.

Sebat has not examined whether the frequency of these CNV mutations increases in aging germ cells — but he suspects it might. “We don’t have data one way or the other,” he says, “but it’s a very tantalizing hypothesis.”

Many of the cellular systems that protect DNA from mutation might begin to fail in aging germ cells, so that their mutation rate increases, Sebat suggests. He is planning to test in a larger group of autistic individuals whether the CNV mutations are more common in children of older parents.

Reichenberg and his colleagues are also testing these hypotheses. In one study, they are trying to compare old and young fathers of autistic children, looking for differences in the rate of new mutations and their association to genetic hotspots previously linked to autism.

They are also doing mouse studies to explore whether offspring of older males tend to suffer more behavioral problems that mimic autism.

There remains some debate about whether the mother’s age is as important a risk factor as that of the father, and studies have differed in their findings. A maternal age effect is harder to tease out, partly because women have children within a more limited age range than men: very few over-40 women have children.

In her study, Croen found that maternal age is just as important and says that other studies have lacked the statistical power to tease this out. “Our data show that maternal age is also in the mix,” she says.

The fact that schizophrenia risk also increases with age leads some researchers to wonder whether some of the same genes may contribute to both disorders – and perhaps to other psychiatric conditions as well.

It’s a “feasible hypothesis”, Reichenberg says, “and I believe a worthwhile one to pursue.”



Malaspina D et al. Arch. Gen. Psychiatry 58, 361-367 (2001) PubMed ↩

Reichenberg A. et al. Arch. Gen. Psychiatry 63, 1026-1032 (2006) PubMed ↩

Croen L. et al. Arch. Pediatr. Adolesc. Med. 161, 334-340 (2007) PubMed ↩

Sebat J. et al. Science 316, 445-449 (2007) PubMed ↩
posted by ApoorvaMandavilliEmail Page


Wednesday, August 13, 2008

Boost Vaccine Safety

Home » Autism News, General » Autism Causes: Boost Vaccine Safety Autism Causes: Boost Vaccine Safety
August 13, 2008 by Not Autism
Filed under Autism News, General
Published on: 08/12/08In recent months, a vitriolic public health debate has been taking place, sparked by the case of Hannah Poling, a 9-year-old Georgia girl with autism. Her parents, neurologist Jon Poling and his wife, Terry, filed in federal no-fault vaccine court, asserting that vaccines caused their daughter’s condition and asking for compensation for the lifelong care Hannah will require.

Without a formal hearing, the federal government conceded the nine vaccines Hannah received on July 19, 2000, significantly aggravated an underlying medical condition — mitochondrial dysfunction, or an impaired functioning of how cells create energy. This predisposed Hannah “to deficits in cellular energy metabolism and manifested as a regressive encephalopathy with features of autism spectrum disorder.” In simple terms, Hannah has autism.

This concession, which became public in March, has prompted strong reactions. Some government officials are, ironically, fueling public distrust of immunizations by failing to acknowledge — much less address — emerging vaccine safety issues. And every day, more parents and some pediatricians reject the vaccination schedule.

Former National Institutes of Health Director Bernadine Healy has entered the debate, saying the scientific community should never turn its back on a hypothesis out of fear for what it might reveal: If you know there is a susceptible group, she said in a television interview, “you can save those children. If you turn your back on the notion there is a susceptible group … what can I say?”

Yet, amazingly, just last month the Federal Interagency Autism Coordinating Committee refused to mention vaccine safety in its strategic plan.

The matter is urgent. One in every 150 children has an autism spectrum disorder. Mitochondrial dysfunction is not rare among these children. The best evidence suggests that at least 4 percent — and perhaps 20 percent or more — of autistic children have mitochondrial dysfunction.

With stakes this high, it’s time for policy-makers to take five common-sense steps to ensure that more children are not damaged by the very vaccines intended to protect them.

• With Marshall Plan dispatch, Congress should launch a bold, nothing-off-the-table program of basic scientific research on the role of mitochondrial dysfunction and neuro-inflammation in autism and other disorders. Funding — $200 million for starters — must not be taken from the Vaccine Injury Compensation Program.

• Reform vaccine practices so they are as safe as possible for both children in general and susceptible subgroups. Examine the schedule, number and frequency of vaccines, use of combination vaccines, preservatives used and ages at which vaccines are administered. Find ways to identify children for whom vaccination or another event might cause or worsen mitochondrial dysfunction, leading to autism. Study siblings to identify biological markers that could lead to prevention, screening and treatment.

• Piggyback new research onto existing efforts. Use the Newborn Screening Saves Lives Act to propel advances concerning genetic and metabolic disorders. Modify the National Children’s Study to test alternate vaccine schedules. And integrate new analyses into ongoing studies, such as mitochondrial research already under way at Johns Hopkins University and the Cleveland Clinic Foundation.

• Identify children nationwide who have abrupt developmental regressions, including those that are vaccine-related, and speed them into research and intense early intervention. And strengthen the Vaccine Adverse Event Reporting System, including imposing serious consequences for health care providers who do not report bad reactions.

• Improve the Vaccine Injury Compensation Program. Encourage parents to focus on early intervention by allowing longer than three years to file. Update the Vaccine Injury Table, making it easier for families to receive compensation as new discoveries emerge. And explore limiting compensation to the most critical immunizations, returning adverse reactions from other vaccines to the regular court system.

A loud wake-up call from a beautiful little redheaded girl from Georgia has provided policy-makers with a historic opportunity to tackle critical issues of vaccine safety. If they fail to answer, what can I say?

— Margaret Dunkle, Hannah Poling’s great-aunt, directs the Early Identification and Intervention Collaborative for Los Angeles County. She is a senior fellow at the Center for Health Services Research and Policy at George Washington University.


Tuesday, August 12, 2008

From Ginger AAP OK to Throw Away 3 per cent of our children



Monday, August 11, 2008

Mutation Causing Mitochondrial Disease More Common Than Previously Believed

New Research Shows One in 200 People Born with DNA Mutation That Can Lead to Devastating, Often Fatal Disease

Last update: 11:20 a.m. EDT Aug. 11, 2008
PITTSBURGH, Aug 11, 2008 /PRNewswire-USNewswire via COMTEX/ -- Mutation Causing Mitochondrial Disease More Common Than Previously Believed
The United Mitochondrial Disease Foundation (UMDF) today announced landmark research finding that one in every 200 people has a DNA mutation that could potentially cause a mitochondrial disease in them or their offspring. Mitochondrial disease is a devastating and often fatal disease, and mitochondrial disorders are at the core of many well known diseases and chronic illnesses, such as Alzheimer's disease, Parkinson's disease and autism spectrum disorders. This research, which was partially funded by UMDF, was conducted by Patrick Chinnery, MBBS, PhD, MRCPath, FRCP, Wellcome Senior Fellow in Clinical Genetics and professor of neurogenetics at Newcastle University in the UK. Dr. Chinnery's findings are published in the current issue of the American Journal of Human Genetics.
"This ground breaking discovery confirms what researchers and experts have believed for some time - mitochondrial disease is not rare," said Charles A. Mohan, Jr., Executive Director and CEO of UMDF. "We now know that 1 in 200 people carry the mutation for this horrible, debilitating disease. This discovery underscores the need for additional research funding to help better diagnose and treat affected individuals and to learn more about how mitochondrial dysfunction is connected to other diseases."
Mitochondrial diseases are extremely complicated and often go undiagnosed or misdiagnosed for years. They develop when the mitochondria - the body's main energy source - do not function properly. Mitochondria are responsible for creating more than 90 percent of the energy needed by the body to sustain life and support growth. Because they are in almost all human cells, this "power failure" results in disease that can affect almost any body tissue. Therefore, the severity of symptoms and how the disease manifests itself can vary from person to person. One person may suffer difficulty breathing, have uncontrollable seizures and/or digestive problems, while another may not be able to walk, talk, see or hear.
"The demonstration by Dr. Chinnery and colleagues that at least one in 200 newborns harbor known pathogenic mitochondrial DNA mutations indicates that mitochondrial dysfunction is a major underlying risk factor for human disease," said Dr. Douglas C. Wallace, Donald Bren Professor of Molecular Medicine, Director of the Center for Molecular and Mitochondrial Medicine and Genetics, University of California-Irvine. "This new observation augments the rapidly expanding body of evidence indicating that common mitochondrial DNA lineages modulate the risk for developing a wide variety of diseases including diabetes, cardiovascular disease, Parkinson Disease, Alzheimer Disease, various cancers, as well as longevity."
The mitochondrial DNA encodes essential genes for mitochondrial energy production. Therefore, mitochondrial dysfunction represents a major unexplored area of human biology of vital importance to human health. Along with the diseases noted above, mitochondrial dysfunction has been implicated in autoimmune diseases such as multiple sclerosis and lupus. While it cannot yet be said that mitochondrial dysfunction causes these problems, it is clear that mitochondria are involved because their function is measurably disturbed.
"Dr. Chinnery's research raises many new questions - none of which can be answered without additional dollars allocated for research into mitochondrial disease and dysfunction," said Mohan. "This line of research holds great promise. Ultimately, the investment we make may enable doctors and researchers to transform medicine, benefiting not only those suffering from mitochondrial disease, but the many millions of Americans who suffer from the wide range of diseases related to mitochondrial dysfunction."
Dr. Chinnery's study was performed on 3000 randomly ascertained neonatal cord blood samples, screening for ten specific DNA mutations related to mitochondrial disease. The study's findings establish that the incidence of new mutations and the frequency of asymptomatic carriers are not rare and emphasize the importance of developing new approaches to prevent transmission.
SOURCE United Mitochondrial Disease Foundation
Copyright (C) 2008 PR Newswire. All rights reserved


Saturday, August 09, 2008

It's A Time Bomb

Article by Tamar Lewin

Ideas & Trends: Reproductive Gerontology; Ask Not for Whom the Clock Ticks!

MEN, take note: you, too, have a biological clock.

True, it does not tick toward the absolute deadline that ends women's childbearing years. As notables like Tony Randall, Yasir Arafat, George Plimpton, Anthony Quinn, Clint Eastwood, Strom Thurmond and so, so many more have demonstrated, men can father babies no matter how old they get.
But there is a growing body of evidence that the fruit of aging loins is burdened with increased risk of a wide variety of gene-influenced illnesses. A study released last week raised the intriguing -- if skeptically viewed -- possibility that some cases of schizophrenia fall into that category.

The study found that older fathers are more likely to have children with schizophrenia. Fathers over 50 have three times the risk of having a child who develops schizophrenia as fathers under 25, the study found. Earlier studies linked advanced paternal age to a variety of conditions, including the most common type of dwarfism, neural tube defects, nervous system cancer, prostate cancer, neurofibromatosis, Apert syndrome (a malformation of the skull, hands and feet) and Marfan syndrome, which involves defects of the eyes, bones, heart and blood vessels. The study does not address what it is about the father that could cause schizophrenia. But Dr. Dolores Malaspina, a researcher at Columbia University and the lead author of the schizophrenia study, said that scientists have been seeing signs of a male biological clock for some time. ''While scientists have known for years that older fathers are a major source of gene mutations,'' she said, ''the public doesn't seem to have absorbed it, which may have something to do with a culture that sees older fathers as triumphantly virile.''

As research continues, her team suggested, it may be that the father's sperm will turn out to play as big a part in children's genetic problems as the mother's eggs.
While women are born with all the eggs they will ever have, the cells that become sperm divide and reproduce throughout a man's life -- with each division introducing a slight risk of error in the genetic material the new sperm passes on to the children. For men in their 40's and 50's, who assumed they could defer parenthood to their later, quieter years, the possibility of a male biological clock is not a happy concept.

''This is a new idea to me, and it doesn't make my day,'' said Gregory Mosher, a New York director and producer. ''But science is so mind-boggling that there always are new discoveries that make you rethink all your assumptions. This is just another thing to talk about with whoever you're making the decision with.''

And some men reacted by pointing out that, if they do have such clocks, they tick quietly. ''I know that the problem women face with their biological clock is something I'll never experience or fully understand,'' said Richard Orloff, a playwright. ''For men, even if there's some higher risk of having a child with a problem, there's still the possibility of being a father.''
If, as the new study suggests, one-fourth of all schizophrenics have older fathers, it may seem puzzling that the correlation was not noticed long ago. But what scientists find depends on what they look for, as women angered by the lack of female-specific data on problems like heart disease have long pointed out.

''We've known since the 1960's that schizophrenia is associated with last-born kids and older parents,'' said Dr. Malaspina. ''But most people choose spouses about their age, and if you didn't look specifically at the father's age, you would think there was a powerful link between maternal age and schizophrenia. It's only when we separated it out that we saw that paternal age mattered, and maternal age didn't.''
There is a particular irony in the finding that the devastating mental illness once thought to be caused by a type of bad mother -- the ''schizophrenogenic'' mother, a staple of 60's psychiatry -- may have something to do with the father.

But the impulse to assess reproductive health by looking solely at the mother is a widespread one. In industry, efforts to keep women out of certain workplaces with dangerous substances have been turned back only with findings that the same substances can harm sperm -- so the better approach is to create an environment that will be safe for men and women alike.
Gloria Steinem, a founder of Ms. magazine, said it has been difficult to focus public attention on the health risks of aging fathers. As long ago as 1976, Ms. ran an article called ''The Older the Sperm . . . .''
''I guess it takes a long time to sink in,'' Ms. Steinem said, ''since our society seems to look to a star in the East, for a baby born to a mother, and no father.''
And that, said Katha Pollitt, a feminist author, reflects the whole history of everything having to do with reproduction,
''The woman is always blamed for everything,'' she said.
While the club of biological clock watchers is not a happy one, some women say there is a certain satisfaction in welcoming male members.
''It's not a totally free ride for men,'' Ms. Pollitt said, ''and that seems fair, that both men and women have lots to think about.''

Isn't that an interesting article? I have a few others to add to that growing list, Rod Stewart, Mick Jagger, Paul McCartney, Donald Trump and Robin Williams.,just to name a few.

That article says it all! What are men thinking? Is it fair to bring kids into the world, knowing they might have serious medical problems later? Is it fair to bring kids into the world knowing you're about to exit?

I sure can identify with that article! My mom met my dad when she was 21 and he was 56., and they proceeded to have 11 kids. Yes, he was a Catholic, so I guess when the church said, 'Go out and multiply', he took them seriously! (okay, the bible!)

Also, the Catholic church did not allow contraception, and yes, the church was in the bedroom in those days. Women were also told that as good wives, they were not to deny their husbands needs.

My dad died when I was 11 years old,,,a middle child! My 2 older brothers were 15 and 16 at the time. My oldest brother didn't want to quit school, he knew that an education would be his ticket out of poverty! The 2nd eldest did quit school and worked at a variety of jobs, grocery delivery boy, drugstore delivery, to help out at home.

We were destitute, no money, no insurance, no savings, but most of all, the stability of a home with a mother and father were now gone. My mother had little education and no training.

I had 7 brothers who had no 'male role model', nobody to tell them right from wrong,,to encourage, teach, to help mold their characters., to show them how a man acted as a husband, a father, a mentor. Nobody to toss a ball with,,nobody to cheer when they did well, nobody to pat them on their back, and say., "You did good, son!"

My 3 sisters and I had no daddy! Girls as well as boys need their dad. A father is a role-model for a girl,,,,,,she first falls in love with daddy before finding and choosing a husband. She will marry someone who was like her dad. Her dad is the one who shows her how she is to be treated and loved by men. If a father treats his daughter well, loves and respects her, that is what she will expect from the men she meets.

We never got to know our dad well; growing up, he was always sick, after all he was an old man!

I do have a few good memories of him; he was a great story teller,,,a good cook, never beat us,,, took great pride in our accomplishments.....but just when we needed him,,,,,,he was gone! We all regret that we had no dad to walk us up the aisle, or see his grandchildren, or give us the advice and love we needed as we grew up.

And that's all we have, a few memories and 2 photograph's.

My younger siblings don't have the few memories I have, after all I was 11, and they were so much younger., so they have no memory of a dad!

And sure enough, I have a brother who is younger than me, who is schizophrenic,,,he was diagnosed at the age of 24, and he is now 54, still battling his demons,,,and a few more in my family who haven't been diagnosed! (Depression, anxiety disorders, delusional), Lord Jumping Jesus! I won't say anymore! Let's not go there!

One point I do want to make is, it seems to me, the girls in my family have faired better than the boys! The boys had no 'male mentor', the girls did!

Add to that,,,sisters who married young,,,,one sister was 13, another sister left home at 15, and one other at 16,,,no, that wasn't stupid on their part,,,,it's called 'survival'...getting out of a bad situation. There's nothing pretty about poverty. Those who say, 'We were poor, but we were happy',,,,are in denial! But of course, there are varying degrees of poor!

Being promiscuous is another factor in not having a dad. The one sister who married at 13, did so because she was pregnant, couldn't even find a priest to marry her. She was married by the Salvation Army, and my mother had to give her permission! A child having children!

If we had a father around, would that have made a difference? I'm absolutely positive it would have!

My mother, a very simple woman, with a 3rd grade education and no work experience was overwhelmed to say the least. A widow at 43 with a brood of 11 kids to take care of and no clue as to how she would do it! She couldn't cook,,,(I wrote about that in my 1st post), she couldn't budget, and being an orphan herself, she didn't know how to raise a family, how to discipline them or nurture them. My dad was the one who told her what to do and how to do it!

Back then, there was no welfare and no family allowance did what you could with what you had!
And my mother did what she could with the tools she had!

Once, when I spoke to my older brother John about our dad, I was surprised and shocked that he was so bitter.

He told me having kids at that age was a very selfish, egotistical act, and he was angry at my dad. He wanted an education, he didn't want to quit school, he loved school, and the weight and responsibility of his mother and siblings were too much for a boy of 16 to bear., and I saw my big brother cry at the injustice of it all!

We managed,,,we survived,,,,but it would have been much easier with a dad around to share in our lives, to be there for us!

And now,,,,just to make it easier for older men to make babies,,,,,,we have Viagra! You wonder why older men are taking younger wives? It's an ego thing,,,they want to leave their mark, their progeny, children to carry their name.

I heard it said, that one day in the future, in a few thousand years, women will no longer need men, so men will become extinct! I'm sorry I won't be here!

Posted by Matty at 6:56:00 PM

Labels: Family.

Kacey said...
I have been worried by the number of American couples who have put off having children until they are ready for their alarm clocks to go off. When they decide to "go forth and multiply" they are too old and tired to keep up with the brats they have created. I know we have all our eggs at birth, but I also know that men's sperm can be contaminated by pot, alcohol and other medications. It would be better if the older dudes would shoot blanks. It's bad enough for them to produce nasty little boogers, but now we find that these kids have two or more personalities.
I find your post very well thought out and you did a great job of tying all the pieces together. Nice job, Matty.

Wednesday, January 10, 2007
Matty said...
I met so many parents with Down Syndrome Children and a good majority of them were older. The sad thing is they were told of the chances when they decided to give birth. It's just not fair to bring these kids into the world knowing that you're about to leave. Who's going take care of these kids and make sure they have a quality life?

Wednesday, January 10, 2007
Anonymous said...
Your younger brother has schizophrenia because of your father's age and it is very fortunate for you and your siblings that he is the only one. An older man's damaged sperm are responsible for most of the "mysterious genetic diseases" and researchers have known of the connection for almost 50 years. It would be best for the parents to complete their biological family by 35-40 at the oldest. Men should freeze semen in their 20s if they are going to put off fathering, in my opinion.
These epidemiologists are trying to warn people, but no one is listening.

James F. Crow Emeritus Genetics professor from the U. of Wisconsin, not studying schizophrenia said,
"I conclude that for a number of diseases the mutation rate increases with age and at a rate much faster than linear. This suggests that the greatest mutational health hazard in the human population at present is fertile old males." This psychiatrist knows about the tragedy of schizophrenia and is concerned about warning the public at some point.:

Saturday, January 27, 2007
Matty said...
Thank you for posting! I never said I only had one brother with schizophrenia,,,,,at one point in my life I had no choice but to get him diagnosed,,,,and that's how we know. I have 2 other brothers who show signs of paranoia schizophreni (who were never diagnosed) but are clearly 'off the wall',,,,,,and another brother who is so self-medicated, it's hard to tell, (he's an alcoholic) and another brother who was 27 when he died,(cause unknown) but he definitely had mental problems.
Those 5 kids were younger than me, I was fortunate, I had bouts of depression which I fought constantly and still do.
It's just plain ignorance and the public is not educated enough.
I will look at those articles you cited.

Saturday, January 27, 2007
Anonymous said...
Matty just wanted you to have a link to my paper.


Friday, February 23, 2007
Matty said...
Thank you for the info. I can see I have a lot of reading to far its very interesting.

Friday, February 23, 2007
Dr. Leonid Gavrilov, Ph.D. said...
Thank you for your interesting post!
I thought perhaps you may also find this related scientific study interesting to you:
Human Longevity and Parental Age at Conception

Saturday, April 21, 2007
Post a Comment

Links to this post


Friday, August 08, 2008

From Age of Autism David Kirby 8 8 8

And Dr. Healy noted, “No research has been done on the vaccine schedule to say it is the right one, compared to other schedules. As far as I know, there have been no randomized trials comparing different vaccine schedules to what is better medically for children.“Are we giving children too many vaccines in a very short period of time, so early in their lives? That is the study that has not been done -- looking at the schedule, looking to see if it is better to spread out some vaccines over a longer period of time.”

If we do such comparison, she said, “Are there fewer side effects, fewer fevers? We have very different schedules that should be compared. Have any of them ever been compared with the current one, in terms of the health effects on children?”

“The fact is,” Dr. Healy concluded, (without launching into a single personal attack against any opponent), “there has never been a randomized trial to see what is best for children in terms of their health.”


Thursday, August 07, 2008

The muscle cells had mitochondria with a "paternal" genetic defect.

The muscle cells had mitochondria with a "paternal" genetic defect.
It is our differences, our diversity which makes all of us, of the same species, who we really are as individuals. Humans are more than 99.9% of us identical

"Truth and morning become light with time." — Ethiopian Proverb
The more sure you are of science or politics the more things change. Just when the facts were about as solid as you thought they could be here comes a different premise.

Scientists in Denmark turned biology on it’s head with what was the accepted wisdom about mitochondria. What you thought you knew about mitochondria was probably wrong if you thought your mitochondria only comes from your mother. It appears there is an exception.

In every cell in your body you have mitochondria, lots of them and the assumption has been you get it from your mother. They are small turbo-charged power generators which appears to be evolved from bacteria (according to a theory by Lynn Margolis a few years ago) which is an organelle which lives outside the nucleus and generates ATP, the fuel necessary for life.

Mitochondria are little energy generators which manufacture the energy we need to live.

These little organelles are as small as bacteria which are one hundred thousand times smaller than your cells. They make ATP which fuels everything in your body. They are so small that you could take a billion of them and easily fit them on a grain of sand.

As often happens with science, theories are constantly being tested and new research improve on those theories. Danish scientists, Marianne Schwartz, a geneticist at Copenhagen University Hospital, et al, have published their research in the New England Journal of Medicine, which document an exception to the assumption that mitochondria is exclusively from mothers. They discovered muscle cells containing paternal mitochondria.

The muscle cells had mitochondria with a "paternal" genetic defect. Other cells; in blood, skin and hair did not have the defect and the genetic pattern indicated they were "maternal" mitochondria.


Wednesday, August 06, 2008

Sporadic Cases of Polycystic Kidney Disease due to germline mutations in older fathers

A tumor necrosis factor-[alpha]-mediated pathway promoting autosomal dominant polycystic kidney disease pp863 - 868
Polycystic kidney disease can be caused by germline mutations in the gene encoding PC2 followed by a second somatic 'hit' in the normal allele. Li and her colleagues now show that TNF-[alpha] can also act as a second hit and that disease progression can be blocked by anti-TNF-[alpha] treatment in an animal model.
Xiaogang Li et al.

Changing Definition of Autism Obfuscates the Paternal Age Cause of Much Non-familial autism and schizophrenia

What's certain is that the DSM definition has become more expansive. In the version of the manual from 1968, the word "autism" appears as a symptom of childhood schizophrenia. It only became its own category in 1980, and in 1987 the diagnosis required a finding of eight social and linguistic impairments rather than six. In 1994, the term Asperger's was introduced so doctors could diagnose a lesser form of the disorder. Awareness is also affecting the diagnosis rate: Clinicians know what to look for and are encouraged to act quickly when they notice symptoms.
Posted by Mari at 9:48 AM

Labels: ,

Maybe Somali polygamy perpetuates possible gene connection to autism

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Refugee resettlement watch

Maybe Somali polygamy perpetuates possible gene connection to autism
Posted by acorcoran on August 5, 2008

"I wrote a post a little over a week ago about how Somali refugee children in America are showing extremely high and unexplained rates of autism for those born in the US. Minnesota schools are seeing these children enter the sytsem and are attempting to cope with the alarming influx.

In our earlier post we cited an article that had a couple of possible suggestions. One was the usual complaint about immunizations and the other was the possibility that the relative lack (compared to Africa) of sunshine in Minnesota (and Sweden where the problem is also appearing) might explain the high rate.

However, this article in a blog called “A War of Illusions” leads to another possible cause for the high rate of autism in Somalis in America. But, first here is what the post says about the situation in Minnesota where a conference will soon take place to address the crisis.

About a quarter of all autism children who attend autism classrooms for students functioning too low to be mainstreamed in regular schoolrooms are Somali. Special education specialists said that indicates that the degree of autism Somali children are developing is on the severe end of the autism spectrum.

“I’m not seeing Aspergers syndrome and the full spectrum of autism in Somali children. It is the more classic forms of autism in general; it is the more severe forms of autism that we’re seeing in our Somali babies that are born here,” said Anne Harrington, early childhood special education coordinator for the Minneapolis district and a specialist on the topic.

“If they’re having more children, many of the siblings also have autism. We have a number of [Somali] families who have two children on the autism spectrum and sometimes more. I’ve been working to get somebody to look at this and pay attention because it feels like this is too specific [to Somalis]. It’s got to be preventable,” Harrington said.

The article also tells us there is a lot of shame in the Somali community associated with families who have autistic children which makes me think that the tough life in Africa may have eliminated some of these children at a young age thus making it appear that somehow their move to the US is responsible for a jump in the numbers.

The blogger then leads us to new research that may show that autism is genetic.

Many cases of autism are caused by genetic defects that disrupt the brain’s ability to learn, according to groundbreaking research that promises to lead to new therapies.

To do the research scientists needed to find large families in which cousins married cousins—they found them in Muslim countries in the Middle East.

Research into autism genetics has been hampered by the difficulty of finding autistic and non-autistic siblings in the same family to study. To get around this, the new study investigated 88 families from the Middle East, Turkey and Pakistan, where the average number of children is much larger than in Europe and America. The scientists also concentrated on families in which the mother and father were cousins, which is a risk factor for autism.

In five families, they found large segments of the genome were missing. Non-autistic members still had one working copy of these regions, but those with autism lacked working copies altogether.

I suggest genetic researchers check these Minnesota Somali families many of whom may be linked by a few polygamous fathers—an Islamic cultural practice creeping into America with the refugees—and a surefire way to spread a defective gene. Or if political correctness hinders that line of questioning, at least check the cousins marrying cousins angle."


Monday, August 04, 2008

Dr. Frank Engley: Farewell to a Truth-Teller By Anne Dachel

Dr. Frank Engley: Farewell to a Truth-Teller
By Anne Dachel

Most of the time, in the countless articles and news videos I look at, the controversy over vaccines and autism is presented as a debate with scientists and doctors on one side and parents along with the general population on the other side. We rarely hear about the experts who challenge the claims of health officials. This is a point of increasing frustration for me and countless others in the autism community.

Sunday, August 03, 2008

From Ginger Taylor #links Lists "Autism" as Known Adverse Reaction to DTaP Vaccine Tripedia

In's "A to Z Drug Facts" section the entry on Diphtheria / Tetanus Toxoids / Acellular Pertussis Vaccine contains the following Central Nervous System Adverse reactions for Sanofi Pasteur's Tripedia:

Drowsiness (29%); irritability (25%); anorexia (10%); fussiness (6%); autism, convulsion, encephalopathy, grand mal convulsion, hypotonia, neuropathy, somnolence (postmarketing)."

Hats off to for actually providing informed consent to consumers. To my knowledge they are the first to do it.

HT: Allison Chapman


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