I am writing today about a law that I feel puts the disabled at a huge disadvantage and that has affected my and my child’s life greatly because of my disability benefit. I have read that other states are now changing these laws and I hope Pennsylvania will be next.

I’ve been disabled for 10+ years, after 10 years of being an RN, having my very first job at the age of 15. I am divorced and have one child. My issue has to do with my child support and the laws of Pennsylvania (and most other states) that govern how child support is determined for someone on SSDI.

Normally, child support is determined by combining both parent’s income and then broken down into a percentage for each parent based on their income. For example, if Mom makes $30,000 and Dad makes $70,000 then Mom is responsible for 30% and Dad is responsible for 70% and would pay that 70% to Mom in monthly child support (if mom has custody of course). In PA, with one child, the total child support would be $1116 and Dad would pay Mom $770 per month.

BUT when SSDI is involved, and the custodial parent receives a check for their dependent child, the amount of that benefit check is subtracted from the TOTAL child support before the total is broken into percentages. Of course, Mom’s income would be much lower on SSDI.

In that case, if Mom’s income is $1500 each month from SSDI and she received a check for her child for $750 each month and Dad still made the $70,000 each year, the total child support would be around $1046 and then the $750 benefit is subtracted ($296) and then Dad would be ordered to pay monthly child support of $227 based on the percentages.

How is it possible that Dad gets this huge decrease in his ordered child support because Mom is suddenly disabled???? It makes no sense!!

My monthly income is $1547 (since they don’t count the $821 as my income) and my child’s father’s income is $10,000 per month, so our combined incomes create a child support total of $1278 total child support each month.

The check I receive for my daughter is deducted from this amount leaving $457 to be paid. Her father pays $321 of this amount and the rest comes from my $1547 each month in the amount of $136 assumed by me.

If you consider the total determined monthly support amount of $1278, my daughter’s father pays $321 which is only 25% of her total support even though his income is FIVE TIMES my income!

If you consider the SSDI check I receive on her behalf and EARNED through years of hard work for my daughter to be my income and add the $136, then 74% of her support comes FROM ME !!

The way the courts have balanced this for the first few years is to allow me to ask for alimony. This is not only humiliating, it has cost me a fortune in legal fees and has created tremendous hostility in my ex-husband as he sees this as me asking for support for me. All I want is to maintain a stable home for our child.

At this point, the original alimony order has expired and I am in the middle of having the case reviewed in the family courts and the alimony ordered once again. We were only married for 5 years, so this is very unlikely. And he, of course, can afford the best of the best attorney who keeps dragging it out and having it delayed as I fall further and further behind on bills each month.

I should NOT have to be asking for alimony to maintain a home for my child. I should get the child support that is deserved and needed to care for my child without this huge expensive battle.

If you are able to help in any way, I would be so eternally grateful, as would hundreds of other parents in Pennsylvania and thousands across our country.

Here is a link to just the beginning of the language I am finding in other states’ laws http://www.childsupportguidelines.com/articles/art200011.html

Some higher court cases have determined that SSDI is earned insurance policy and the benefits paid are income replacement, so the disabled, custodial parent should count the benefit for her child as her income and support should be calculated from there. That would mean that $821 should not be deducted from the equation as shown above but should be counted as earned income by me, as her mother.

If that were the case, her monthly child support total would be $1323 according to the PA calculators. My share would be 23% and his would be 77% based on our monthly incomes.

That would mean his share would be $1018 ordered monthly automatically and mine would be $305. Most importantly, it would mean my daughter would grow up in the home I’ve created for her without the worry of not being able to afford the home.

I am praying that someone will help those of us who can not afford to help ourselves.

Thank you for your time and consideration,
Leslie Ann Carlins

We battled Cigna and PG for 2 years. Mike wanted to go back to work, so he would try. Cigna wanted to deny the claim, so they would try. It was an emotionally exhausting battle. Mike tried everything from Hyperbaric Oxygen Therapy to injecting chemo into his belly once a week. (as he does now as well as Cimzia). Ultimately 4 specialist came to the agreement that the only way Mike will keep his leg is to stay on permanent disability.

Through this battle to find relief Mike also developed Vascular disease, a “massive” dvt. Besides Osteoporosis.

December 2009 Mike moved onto Long Term Disability. They notified of a review in March. Then denied his claim in May 2010 without notice. Cigna has been told by 3 specialist since November of 2009, that Mikes conditions are chronic and dibilating and these diagnosis’ will not change. They have been told that any trauma to his leg WILL lead to amputation. These facts were made aware to them yet again in May. They still chose to deny his claim. They have been made aware of his limitations. They have a colonoscopy report from 7/2009 proving that is Crohn’s is active, yet in May 2010 that was not “current” enough. They have said to him they look for “weight loss” to prove that Crohn’s is active. They also want labs for PG. According to their own medical encyclopedia, there are no labs for PG.

This company has lost DR. notes. (the colonoscopy report had to be faxed 3 times). They have ignored diagnosis’ and prognosis’ repeatedly. They do not return phone calls from us or our Dr.s. They have said they have phoned Dr.s when they have not.

My husband did not ask to be sick. He is only 45 years old and he loved his job. Cigna is a horrible company. If we knew this is how he was going to be treated we would have been better off burning the money he spent on premiums in the back yard.

A special May issue of the Journal of Alzheimer’s Disease, guest editors Judith Miklossy, from The University of British Columbia, and Ralph N. Martins, from Edith Cowan University and Hollywood Private Hospital, Perth, Western Australia, and a group of experts explore the topic of how pathogens may suppress, subvert or evade host defenses and establish chronic or latent infection, which has received little attention in the past.

It appears that during an infection cells generated by inflammatory cells may cause DNA damage. Depending upon the biology of the pathogen and the host defense mechanisms the organism can persist in the infected tissues and cause chronic inflammation and amyloid plaque. The outcome of infection is as much determined by the genetic predisposition of the patient as by the virulence and biology of the infecting agent.

This special issue contains a series of reviews from both a historical and recent perspective. The first review shows the importance of chronic inflammation in AD, followed by three articles presenting evidence on the involvement of spirochetes, Chlamydia pneumonia and Herpes simplex virus type 1 in Alzheimer’s disease. These are followed by a review of amyloid proteins, which occur in many cellular forms in Eukaryotes and Prokaryotes.

The editors feel that treatment of a bacterial infection and associated viral infection may result in regression and, if started early, prevention of disease. The impact on reducing health-care costs would be substantial.

Donna Kritz-Silverstein, PhD, adjunct professor, Family & Preventive Medicine, University of California, San Diego, and colleagues, studied effects of DHEA supplements on 110 men and 115 women, between 55-85. The participants received either 50 mg doses of DHEA or a look-a-like placebo. Six cognitive function tests were given and measures of depression, perceptions of physical and emotional health, life satisfaction and sexual function were recorded at the beginning of the study and again at the conclusion of the study one year later.

Although the group receiving DHEA had returned to youthful levels of the drug there were no benefits for cognitive function. Also, there were no differences seen between those taking DHEA and those taking placebo in quality-of-life measurement scores.

Previous clinical trials examining the effects of DHEA supplementation on cognitive function and quality-of-life have inconsistent results, with some showing positive effects and others showing no effect. However, these trials used small sample sizes, were of short duration (generally 2 weeks to 4 months) and did not include older men and women who were at an age when memory loss and cognitive impairment become more apparent. Also, unlike the participants in the majority of previous studies, the participants in this study were not selected for lower levels of DHEA, meaning the results reflect what would be found in the general population.

The study is published in the Journal of American Geriatrics Society.

William Bowers, associate professor of neurology, microbiology, and immunology, University of Rochester Medical Center, believes he and his co-workers have demonstrated a way to create a potent, but safe, version of a vaccine that causes an immune response that prevents Alzheimer’s disease and memory deficits.

Mice, genetically engineered to develop Alzheimer’s, were given a vaccine that caused the immune system to target amyloid beta proteins–considered to be the cause for Alzheimer’s disease. Previous to the 10-month study the mice were trained to navigate through a maze. During the study the mice were timed on how long it took to successfully get to the maze’s exit. The maze test results excited researchers because it indicated their vaccine was able to prompt the immune system to successfully remove amyloid beta before it mutated into the Alzheimer’s disease causing form.

A number of studies will be needed to meet regulatory requirements before the vaccine can be tested on humans, which is expected to take at least 3 years.

Shirley E. Poduslo, PhD, neuroscientist, Medical College of Georgia Schools of Medicine and Graduate Studies, studied the genetic profile of 2 large Georgia families with high rates of late-onset Alzheimer’s disease. Poduslo was shocked when she found that the single nucleotide polymorphisms (SNP) occurred 9 out of 10 times in affected family members. SNPs also were found in the DNA of 36% of 200 late-onset patients stored in the Alzheimer’s DNA Bank.

The gene variation was in the TRPC4AP; part of a large family of genes that is not well-studied, but believed to regulate calcium. Calcium is needed throughout the body and its dysregulation can result in inflammation, nerve cell death and possibly plaque formation.

The next step is to identify the specific genetic mutation responsible. The mutation could be a deletion of some of the nucleotides, an insertion into the gene, or something that prevents the gene from duplicating correctly.

James Shorter, PhD, Assistant Professor of Biochemistry and Biophysics, University of Pennsylvania School of Medicine, has made a surprising discovery. A small molecule, called DAPH, can be used to target the areas that hold the amyloid fibers together and convert the fibers to a form that makes them unable to grow. DAPH accomplishes this remarkable goal by preventing growth from the ends of the fibers.

The DAPH molecule remodels the fiber architecture, which is something researchers have not been able to accomplish before. DAPH was originally found in a screen of small molecules that reduce amyloid-beta toxicity by Vernon Ingram, Massachusetts Institute of Technology (MIT), and co-researcher.

When a small amount of amyloid (or prion) fiber is added to the normal form of the protein it is converted to the fiber form. However, when DAPH is added the conversion process is prevented and essentially stops fiber formation in its tracks.

Some types of amyloids may be helpful–like in formation of memories–so, researchers are now looking for a way to selectively choose which type of amyloid protein is affected.

The Alzheimer’s Disease Anti-Inflammatory Prevention Trial (ADAPT) Research Group studied 2,117 individuals, 70 years and older, who have a family history of Alzheimer’s. For 3 years the participants were tested annually for cognitive function.

• 29% were given 200 milligrams of celecoxib twice daily.
• 28% were given 220 milligrams of naproxen sodium twice daily.
• 43% were given a placebo.

Six months after the study was terminated (because another study found celecoxib increased cardiovascular risks) the use of NSAIDs did not show a protective effect and in fact naproxen users had a lower cognitive assessment score when compared to celecoxib and the placebo.

Why the difference? Several explanations were offered:

• Previous studies analyzed behavior rather than assigning subjects to treatment groups.
• Factors not measured in the previous study may have confounded or affected the results.
• The findings of this study apply only to celecoxib and naproxen.
• NSAIDs may be protective only when given several years before the decline of cognitive function.

Researchers conclude that naproxen and celecoxib should not be used for the prevention of Alzheimer’s disease.

In an article published in the Annals of the Rheumatic Diseases a study reports that researchers compared 136 women with rheumatoid arthritis with 544 women of a similar age without the disease. They found that those who had breast fed for longer were much less likely to get rheumatoid arthritis.

Women who had breastfed for 13 months or more were half as likely to get rheumatoid arthritis as those who had never breast fed. Those who had breast fed for one to 12 months were 25% less likely to get the disease.

The proportion of women breast feeding for more than six months has increased dramatically over the past 30 years. The authors concluded that it was difficult to say whether there was a connection between higher rates of breast feeding and a corresponding fall in the number of women affected by rheumatoid arthritis, but that the results of the study provided yet another reason why women should continue breast feeding.