Posts
The New Mexico Insurance Division is responsible for regulating all types of insurance sold in the state of New Mexico - including health insurance policies.
If you are looking for health insurance coverage, the Insurance Division can help you find an insurance agent or insurance company that is licensed to do business in New Mexico. You can contact them at the phone number listed below.
If you are having trouble resolving a claims dispute with your insurer, you can file a complaint with the Insurance Division. There are separate complaint forms for those who have managed care plans (HMO/PPO) and those who have indemnity insurance. If you are not sure whether you have managed care or an indemnity plan, contact the Insurance Division for help.
New Mexico Insurance Division
P.E.R.A. Bldg., 4th Floor
1120 Paseo de Peralta
Santa Fe, NM 87501
Phone: 505-827-4601 or 800-947-4722
U.S. Department of Labor
If you get your insurance through your job, your plan is also regulated by the U.S. Department of Labor's Employee Benefits Security Administration (EBSA). They make and enforce the rules that your employer must follow when offering health insurance coverage to employees - for example, your employer cannot single out an individual employee to exclude her from the plan because she (or one of her dependents) has a costly illness. Also, if there are 20 or more employees at your job, you should be offered COBRA continuation coverage when you leave your job. The EBSA works to make sure that all of this happens and your rights are protected.
If you have concerns about your employer's practices in administering your job-based health coverage - for example, if you think you should have been offered COBRA continuation coverage, but were not, or if you feel that you were wrongly terminated from your health plan - contact your regional EBSA office.
U.S. Department of Labor Employee Benefits Security Administration
Dallas Regional Office
525 South Griffin Street, Room 900
Dallas, TX 75202-5025
Roger Hilburn - Director
Phone: 972-850-4500
Fax: 214-767-1055
Buying Individual Policies in New Mexico
As a general rule, insurers in New Mexico are allowed to reject your application for coverage based on your health status. However, you may qualify for coverage as a "HIPAA-eligible" individual if you:
* had at least 18 months of continuous creditable coverage, the last day of which was under a group plan AND
* you have exhausted all COBRA continuation coverage which was available to you.
People who are HIPAA-eligible are guaranteed the right to buy insurance through the New Mexico Medical Insurance Pool (described below). If you are not sure whether you are a HIPAA-eligible individual, your insurance agent or the Insurance Division can help you find out.
New Mexico Medical Insurance Pool (NMMIP)
NMMIP offers coverage to individuals who are unable to purchase an individual health insurance policy because they have pre-existing health conditions. It also covers "HIPAA-eligible" individuals as described above. The NMMIP website has information on their eligibility requirements, as well as current premium rates and benefit packages.
New Mexico Medical Insurance Pool
P.O. Box 1594
Roswell, NM, 88201
Phone: 505-622-4711
New MexiKids - the State Children's Health Insurance Program
NewMexiKids provides health insurance coverage for children under age 19 whose family income is between 185% and 235% of the federal poverty level.
New MexiKids
New Mexico Human Services Department
2009 S. Pacheco, Pollon Plaza
Santa Fe, NM 87504
Phone: 888-997-2583
New Mexico Benefits Counseling Program
The New Mexico Benefits Counseling Program provides free one-on-one counseling for Medicare beneficiaries with questions about any aspect of Medicare, including the Medicare Part D prescription drug benefit, or Medigap coverage.
New Mexico Benefits Counseling Program
Phone: 866-451-2901
New Mexico Medicaid
Medicaid is a government program designed to help the poor and indigent obtain health care services. Pregnant women and children under age 19 who meet certain income requirements may be eligible for Medicaid coverage, along with aged, blind, and disabled individuals. For more information about New Mexico Medicaid
Custom Search
Making A Bigger Splash In The Gene Pool
We humans have a strong urge to reproduce, but if the environment steers us into putting off having children, we may be rewarded with both longer life and a bigger genetic footprint in future generations.
So concludes a new University of Minnesota study that reveals what may be a major force in shaping the evolution of most living things, including humans. Harnessing this natural effect could open the door to new means of delaying reproduction while promoting longer, healthier lives.
The work, led by ecology, evolution and behavior graduate student Will Ratcliff, was published online June 25 in the Public Library of Science.
The basic idea is simple. When environmental cues like food shortages signal that the population is about to shrink, individuals who can afford to wait until this has happened should do so; then their offspring, when they come, will represent a bigger fraction of the gene pool.
"When the population is declining, future kids make a greater splash in the gene pool than current kids," Ratcliff explains. "If there are tradeoffs between reproducing now versus later, delaying can be a good idea even if it reduces the number of kids you have during your lifetime."
Conversely, if hard times turn to good times and the population is about to boom, it's better to get those kids out there sooner, while the population is still small.
Rules of the waiting game
Over evolutionary history, early reproduction has reduced life expectancy due to the risk of complications in pregnancy, death in childbirth, damaging fights for mates or social status, and the demands of caring for and protecting offspring, says Ratcliff. Though lessened for modern humans, these risks shaped the evolution of our responses to stress.
For example, in some parts of Africa that suffer chronic food shortages--an environmental signal that the population will decline--girls experience their first menstrual period at later ages.
"Delaying reproduction to age 16 instead of 12 can really increase your chances, and your offspring's chances, of survival because having children very young is fraught with risk," says Ratcliff.
But in Western countries where girls have been getting richer food in recent years, the age of menarche has been receding. Rich food is an environmental signal that the population is poised to rise, and so the age of fertility has dropped.
Besides food availability, the environment may signal an imminent population decline chemically. Many food plants produce toxins that tend to depress reproduction and extend the lifespan. Humans may have eaten more of such plants when meat and other rich foods were relatively scarce, a sign that a population is facing a decline.
"A lot of these toxins extend life in ways that mimic dietary restrictions and have been shown to extend life in mice, fruit flies, roundworms, and yeast," says Ratcliff. "The whole point is that if a population is headed downhill, an individual who trades early reproduction for longevity can come out ahead."
One mechanism may involve testosterone, which suppresses the immune system, says R. Ford Denison, Ratcliff's faculty adviser and adjunct professor in the University's College of Biological Sciences. Thus, a toxin or other cue that reduces testosterone levels would tend to extend life as well as dampen reproductive behavior. Someday, the researchers say, harbingers of population decline may result in new drugs or lifestyle changes that lead to delayed reproduction and, potentially, longer and healthier lives.
What counts is the message organisms get from the environment, not necessarily the actual situation, the researchers say. For example, while the stress of regular fasting can delay reproduction and extend life, animal experiments have shown that the mere odor of food can reverse this effect.
Other authors of the paper were graduate student Peter Hawthorne and professor Michael Travisano of the Department of Ecology, Evolution and Behavior.
So concludes a new University of Minnesota study that reveals what may be a major force in shaping the evolution of most living things, including humans. Harnessing this natural effect could open the door to new means of delaying reproduction while promoting longer, healthier lives.
The work, led by ecology, evolution and behavior graduate student Will Ratcliff, was published online June 25 in the Public Library of Science.
The basic idea is simple. When environmental cues like food shortages signal that the population is about to shrink, individuals who can afford to wait until this has happened should do so; then their offspring, when they come, will represent a bigger fraction of the gene pool.
"When the population is declining, future kids make a greater splash in the gene pool than current kids," Ratcliff explains. "If there are tradeoffs between reproducing now versus later, delaying can be a good idea even if it reduces the number of kids you have during your lifetime."
Conversely, if hard times turn to good times and the population is about to boom, it's better to get those kids out there sooner, while the population is still small.
Rules of the waiting game
Over evolutionary history, early reproduction has reduced life expectancy due to the risk of complications in pregnancy, death in childbirth, damaging fights for mates or social status, and the demands of caring for and protecting offspring, says Ratcliff. Though lessened for modern humans, these risks shaped the evolution of our responses to stress.
For example, in some parts of Africa that suffer chronic food shortages--an environmental signal that the population will decline--girls experience their first menstrual period at later ages.
"Delaying reproduction to age 16 instead of 12 can really increase your chances, and your offspring's chances, of survival because having children very young is fraught with risk," says Ratcliff.
But in Western countries where girls have been getting richer food in recent years, the age of menarche has been receding. Rich food is an environmental signal that the population is poised to rise, and so the age of fertility has dropped.
Besides food availability, the environment may signal an imminent population decline chemically. Many food plants produce toxins that tend to depress reproduction and extend the lifespan. Humans may have eaten more of such plants when meat and other rich foods were relatively scarce, a sign that a population is facing a decline.
"A lot of these toxins extend life in ways that mimic dietary restrictions and have been shown to extend life in mice, fruit flies, roundworms, and yeast," says Ratcliff. "The whole point is that if a population is headed downhill, an individual who trades early reproduction for longevity can come out ahead."
One mechanism may involve testosterone, which suppresses the immune system, says R. Ford Denison, Ratcliff's faculty adviser and adjunct professor in the University's College of Biological Sciences. Thus, a toxin or other cue that reduces testosterone levels would tend to extend life as well as dampen reproductive behavior. Someday, the researchers say, harbingers of population decline may result in new drugs or lifestyle changes that lead to delayed reproduction and, potentially, longer and healthier lives.
What counts is the message organisms get from the environment, not necessarily the actual situation, the researchers say. For example, while the stress of regular fasting can delay reproduction and extend life, animal experiments have shown that the mere odor of food can reverse this effect.
Other authors of the paper were graduate student Peter Hawthorne and professor Michael Travisano of the Department of Ecology, Evolution and Behavior.
Today's Healthcare
Coffee drinkers may have another reason to pour that extra cup. When aged mice bred to develop symptoms of Alzheimer's disease were given caffeine – the equivalent of five cups of coffee a day – their memory impairment was reversed, report University of South Florida researchers at the Florida Alzheimer's Disease Research Center.
Back-to-back studies published online July 6 in the Journal of Alzheimer's Disease, show caffeine significantly decreased abnormal levels of the protein linked to Alzheimer's disease, both in the brains and in the blood of mice exhibiting symptoms of the disease. Both studies build upon previous research by the Florida ADRC group showing that caffeine in early adulthood prevented the onset of memory problems in mice bred to develop Alzheimer's symptoms in old age.
"The new findings provide evidence that caffeine could be a viable 'treatment' for established Alzheimer's disease, and not simply a protective strategy," said lead author Gary Arendash, PhD, a USF neuroscientist with the Florida ADRC. "That's important because caffeine is a safe drug for most people, it easily enters the brain, and it appears to directly affect the disease process."
Based on these promising findings in mice, researchers at the Florida ADRC and Byrd Alzheimer's Center at USF hope to begin human trials to evaluate whether caffeine can benefit people with mild cognitive impairment or early Alzheimer's disease, said Huntington Potter, PhD, director of the Florida ADRC and an investigator for the caffeine studies. The research group has already determined that caffeine administered to elderly non-demented humans quickly affects their blood levels of β-amyloid, just as it did in the Alzheimer's mice.
"These are some of the most promising Alzheimer's mouse experiments ever done showing that caffeine rapidly reduces beta amyloid protein in the blood, an effect that is mirrored in the brain, and this reduction is linked to cognitive benefit," Potter said. "Our goal is to obtain the funding needed to translate the therapeutic discoveries in mice into well-designed clinical trials."
Arendash and his colleagues became interested in caffeine's potential for treating Alzheimer's several years ago, after a Portuguese study reported that people with Alzheimer's had consumed less caffeine over the last 20 years than people without the neurodegenerative disease. Since then, several uncontrolled clinical studies have reported moderate caffeine consumption may protect against memory decline during normal aging. The highly controlled studies using Alzheimer's mice allowed researchers to isolate the effects of caffeine on memory from other lifestyle factors such as diet and exercise, Arendash said.
The just-published Florida ADRC study included 55 mice genetically altered to develop memory problems mimicking Alzheimer's disease as they aged. After behavioral tests confirmed the mice were exhibiting signs of memory impairment at age 18 to 19 months – about age 70 in human years – the researchers gave half the mice caffeine in their drinking water. The other half got plain water. The Alzheimer's mice received the equivalent of five 8-oz. cups of regular coffee a day. That's the same amount of caffeine – 500 milligrams -- as contained in two cups of specialty coffees like Starbucks, or 14 cups of tea, or 20 soft drinks.
At the end of the two-month study, the caffeinated mice performed much better on tests measuring their memory and thinking skills. In fact, their memories were identical to normal aged mice without dementia. The Alzheimer's mice drinking plain water continued to do poorly on the tests.
In addition, the brains of the caffeinated mice showed nearly a 50-percent reduction in levels of beta amyloid, a substance forming the sticky clumps of plaques that are a hallmark of Alzheimer's disease. Other experiments by the same investigators indicate that caffeine appears to restore memory by reducing both enzymes needed to produce beta amyloid. The researchers also suggest that caffeine suppresses inflammatory changes in the brain that lead to an overabundance of beta amyloid.
Since caffeine improved the memory of mice with pre-existing Alzheimer's, the researchers were curious to know if it might further boost the memory of non-demented (normal) mice administered caffeine from young adulthood through old age. It did not. Control mice given regular drinking water throughout their lives performed as well on behavioral tests in old age as normal mice who received long-term caffeine treatment, Arendash said. "This suggests that caffeine will not increase memory performance above normal levels. Rather, it appears to benefit those destined to develop Alzheimer's disease."
The researchers do not know if an amount lower than the 500 mg. daily caffeine intake received by the Alzheimer's mice would be effective, Arendash said. For most individuals, however, this moderate level of caffeine intake poses no adverse health effects, according to both the National Research Council and the National Academy of Sciences. Nonetheless, Arendash said, individuals with high blood pressure or those who are pregnant should limit their daily caffeine intake.
If larger, more rigorous clinical studies confirm that caffeine staves off Alzheimer's in humans, as it does in mice, this benefit would be substantial, Arendash said. Alzheimer's disease attacks nearly half of Americans age 85 and older, and Alzheimer's and other dementias triple healthcare costs for those age 65 and older, according to the Alzheimer's Association.
In addition to the Florida ADRC, Byrd Alzheimer's Center and Eric Pfeiffer Suncoast Alzheimer's and Gerontology Center at USF, researchers from the Bay Pines VA Healthcare System; Saitama Medical University, Saitama, Japan; and Washington University School of Medicine, St. Louis, collaborated on the research. The studies were supported by grants to investigators in the Florida ADRC, a statewide project sponsored by the National Institute on Aging and housed at the University of South Florida's Byrd Alzheimer's Center.
Back-to-back studies published online July 6 in the Journal of Alzheimer's Disease, show caffeine significantly decreased abnormal levels of the protein linked to Alzheimer's disease, both in the brains and in the blood of mice exhibiting symptoms of the disease. Both studies build upon previous research by the Florida ADRC group showing that caffeine in early adulthood prevented the onset of memory problems in mice bred to develop Alzheimer's symptoms in old age.
"The new findings provide evidence that caffeine could be a viable 'treatment' for established Alzheimer's disease, and not simply a protective strategy," said lead author Gary Arendash, PhD, a USF neuroscientist with the Florida ADRC. "That's important because caffeine is a safe drug for most people, it easily enters the brain, and it appears to directly affect the disease process."
Based on these promising findings in mice, researchers at the Florida ADRC and Byrd Alzheimer's Center at USF hope to begin human trials to evaluate whether caffeine can benefit people with mild cognitive impairment or early Alzheimer's disease, said Huntington Potter, PhD, director of the Florida ADRC and an investigator for the caffeine studies. The research group has already determined that caffeine administered to elderly non-demented humans quickly affects their blood levels of β-amyloid, just as it did in the Alzheimer's mice.
"These are some of the most promising Alzheimer's mouse experiments ever done showing that caffeine rapidly reduces beta amyloid protein in the blood, an effect that is mirrored in the brain, and this reduction is linked to cognitive benefit," Potter said. "Our goal is to obtain the funding needed to translate the therapeutic discoveries in mice into well-designed clinical trials."
Arendash and his colleagues became interested in caffeine's potential for treating Alzheimer's several years ago, after a Portuguese study reported that people with Alzheimer's had consumed less caffeine over the last 20 years than people without the neurodegenerative disease. Since then, several uncontrolled clinical studies have reported moderate caffeine consumption may protect against memory decline during normal aging. The highly controlled studies using Alzheimer's mice allowed researchers to isolate the effects of caffeine on memory from other lifestyle factors such as diet and exercise, Arendash said.
The just-published Florida ADRC study included 55 mice genetically altered to develop memory problems mimicking Alzheimer's disease as they aged. After behavioral tests confirmed the mice were exhibiting signs of memory impairment at age 18 to 19 months – about age 70 in human years – the researchers gave half the mice caffeine in their drinking water. The other half got plain water. The Alzheimer's mice received the equivalent of five 8-oz. cups of regular coffee a day. That's the same amount of caffeine – 500 milligrams -- as contained in two cups of specialty coffees like Starbucks, or 14 cups of tea, or 20 soft drinks.
At the end of the two-month study, the caffeinated mice performed much better on tests measuring their memory and thinking skills. In fact, their memories were identical to normal aged mice without dementia. The Alzheimer's mice drinking plain water continued to do poorly on the tests.
In addition, the brains of the caffeinated mice showed nearly a 50-percent reduction in levels of beta amyloid, a substance forming the sticky clumps of plaques that are a hallmark of Alzheimer's disease. Other experiments by the same investigators indicate that caffeine appears to restore memory by reducing both enzymes needed to produce beta amyloid. The researchers also suggest that caffeine suppresses inflammatory changes in the brain that lead to an overabundance of beta amyloid.
Since caffeine improved the memory of mice with pre-existing Alzheimer's, the researchers were curious to know if it might further boost the memory of non-demented (normal) mice administered caffeine from young adulthood through old age. It did not. Control mice given regular drinking water throughout their lives performed as well on behavioral tests in old age as normal mice who received long-term caffeine treatment, Arendash said. "This suggests that caffeine will not increase memory performance above normal levels. Rather, it appears to benefit those destined to develop Alzheimer's disease."
The researchers do not know if an amount lower than the 500 mg. daily caffeine intake received by the Alzheimer's mice would be effective, Arendash said. For most individuals, however, this moderate level of caffeine intake poses no adverse health effects, according to both the National Research Council and the National Academy of Sciences. Nonetheless, Arendash said, individuals with high blood pressure or those who are pregnant should limit their daily caffeine intake.
If larger, more rigorous clinical studies confirm that caffeine staves off Alzheimer's in humans, as it does in mice, this benefit would be substantial, Arendash said. Alzheimer's disease attacks nearly half of Americans age 85 and older, and Alzheimer's and other dementias triple healthcare costs for those age 65 and older, according to the Alzheimer's Association.
In addition to the Florida ADRC, Byrd Alzheimer's Center and Eric Pfeiffer Suncoast Alzheimer's and Gerontology Center at USF, researchers from the Bay Pines VA Healthcare System; Saitama Medical University, Saitama, Japan; and Washington University School of Medicine, St. Louis, collaborated on the research. The studies were supported by grants to investigators in the Florida ADRC, a statewide project sponsored by the National Institute on Aging and housed at the University of South Florida's Byrd Alzheimer's Center.
Subscribe to:
Posts (Atom)
Registration of your site
