From Geriatric Pharmacy Intern, Amalia Castro, PharmD(c)
Nova Southeastern University School of Pharmacy
A new study shows that cutting back on calories reduces aging, as well as, the incidence of age related diseases such as cardiovascular disease, cancer and preserves the brain in primates. Scientists at the University of Wisconsin-Madison performed the study for a period of 20 years. Study author Ricki J. Colman, PhD, reports that this was the largest and the most highly controlled study showing the benefits of calorie restriction on disease prevention and increased survival. He also believes that the results of this study can be applied to humans due to the close relationship between both primates and humans. The study reveals that only 50% of the monkeys that were allowed to eat freely survived, while 80% of the monkeys eating the same foods, but with a 30% calorie reduction, continue to exist.
Richard Wiendruch, PhD, professor of medicine at the University of Wisconsin-Madison School of Medicine and co-author of the study, states that a calorie restricted diet can lead to a longer life span and improve quality of life in old age, as seen with the primates. The study proved an increase in survival by reporting that the incidence of cardiovascular disease and cancer was twice as much for the monkeys on the unrestricted diet. Wiendruch also reports that surprisingly only 42% of the primates on the unrestricted diet had diabetes or pre-diabetes, while none of the monkeys on the calorie restricted diet showed any signs of this disease. This last finding is astonishing and is worth studying on human subjects.
As far as avoiding brain atrophy, the study revealed that the monkeys that consumed fewer calories where able to preserve regions of their brain responsible for short-term memory and problem solving, which are greatly affected with age. The study also showed that a restricted diet appears to have an effect on brain mass. Nevertheless, more studies need to be conducted on these findings, especially on the effects of a calorie-restricted diet and the lack of brain shrinkage.
More information on this topic can be found on the July issue of Science.
Sunday, July 26, 2009
Wednesday, July 15, 2009
Vitamin Toxicity: How much is too much?
Many of us believe that taking abundant amounts of vitamins cannot harm us. This is true for some vitamins like C and B. When we take too much of those vitamins we just urinate the excess. However, there are 4 vitamins which are stored in fat. The vitamins stored in fat (aka fat-soluble) are A, D, E and K. All of them are components in multivitamins. When these fat-soluble vitamins are taken in excess, there may be serious consequences.
Vitamin D is being used by many in the ageing population to prevent or to treat osteoporosis. We can find vitamin D in milk, orange juice, multivitamins and most calcium tablets. It is also found in prescription medications like Fosamax-D. Our bodies also produce it when we are exposed to sunlight. The recommended daily allowance (RDA) is 1000IU. When a person takes in more than this on a daily basis they are at risk for high blood pressure, nausea, vomiting and lack of appetite.
Vitamin A is found in multivitamins, spinach, carrots, leafy vegetables, pumpkin and pretty much any fruit or vegetable with an orange tint. It is used to preserve our vision, immune and reproductive systems. It is also found in prescription medications used for acne as isotretinoin. The RDA is 5000IU. Overdose causes hair loss, dry skin, nasal irritation, fever, insomnia, fatigue, weight loss, anemia and diarrhea.
Vitamin E is used to boost the immune system, as an antioxidant and to protect the skin. Vitamin E can be obtained from asparagus, avocado, eggs, milk, nuts, spinach, vegetable oil and whole grain foods. The RDA is 30IU. It is also supplied in multivitamins.
Vitamin K helps our bodies clot blood and is used to reverse Warfarin overdose. Sources of vitamin K include green, leafy vegetables, cauliflower, brussel sprouts and cabbage. Just like the others, it is found in multivitamins. The RDA is 75mcg. This vitamin and its amount is important in patients taking Coumadin or warfarin. Overdose can cause our clotting system to go haywire.
The majority of the effects listed were of a milder form. The take home point is to attempt to regulate how much of these vitamins you consume on a daily basis and to recognize the signs and symptoms of overdose.
Vitamin D is being used by many in the ageing population to prevent or to treat osteoporosis. We can find vitamin D in milk, orange juice, multivitamins and most calcium tablets. It is also found in prescription medications like Fosamax-D. Our bodies also produce it when we are exposed to sunlight. The recommended daily allowance (RDA) is 1000IU. When a person takes in more than this on a daily basis they are at risk for high blood pressure, nausea, vomiting and lack of appetite.
Vitamin A is found in multivitamins, spinach, carrots, leafy vegetables, pumpkin and pretty much any fruit or vegetable with an orange tint. It is used to preserve our vision, immune and reproductive systems. It is also found in prescription medications used for acne as isotretinoin. The RDA is 5000IU. Overdose causes hair loss, dry skin, nasal irritation, fever, insomnia, fatigue, weight loss, anemia and diarrhea.
Vitamin E is used to boost the immune system, as an antioxidant and to protect the skin. Vitamin E can be obtained from asparagus, avocado, eggs, milk, nuts, spinach, vegetable oil and whole grain foods. The RDA is 30IU. It is also supplied in multivitamins.
Vitamin K helps our bodies clot blood and is used to reverse Warfarin overdose. Sources of vitamin K include green, leafy vegetables, cauliflower, brussel sprouts and cabbage. Just like the others, it is found in multivitamins. The RDA is 75mcg. This vitamin and its amount is important in patients taking Coumadin or warfarin. Overdose can cause our clotting system to go haywire.
The majority of the effects listed were of a milder form. The take home point is to attempt to regulate how much of these vitamins you consume on a daily basis and to recognize the signs and symptoms of overdose.
Friday, July 10, 2009
Statin use and Alzheimer's Disease
From Geriatric Pharmacy Intern, Amalia Castro, PharmD(c)
Nova Southeastern University College of Pharmacy
According to the Alzheimer’s Association, Alzheimer’s disease is the seventh leading cause of death in the United States and affects more than 5 million Americans. This neurodegenerative disease targets brain cells causing irreversible damage and neuronal cell death, which results in severe memory impairment and radical changes in behavior. The Alzheimer’s Association also states that it is the most common form of dementia, accounting for 50 to 70 percent of dementia cases. Currently, this eventually fatal disease has no cure, and only symptomatic treatment and supportive care are offered to these patients in order to improve their quality of life. Consequently, it comes as no surprise that the struggle to find a way to reverse or eradicate this disease is crucial.
Recent promising studies show that statins, a class of commonly used cholesterol lowering drugs, may help protect brain cells against excitotoxicity, which consists on overstimulation of nerve cells, eventually leading to cell death. Overstimulation is the leading cause of degeneration of nerve cells in Alzheimer’s patients.
Lovastatin was the cholesterol reducing statin used in animal studies done by Amalia Dolga, PhD and her colleagues at the University of Groningen in the Netherlands. Her study showed that besides reducing cholesterol, Lovastatin was able to protect nerve cells against damage caused by overstimulation. By avoiding damage on nerve cells we can extend their memory capacity, avoid their deterioration and cell death caused by Alzheimer’s disease.
On her previous in vitro Lovastatin study, Dolga and colleagues were able to demonstrate this dug’s neuroprotection ability through the activation of the tumor necrosis factor (TNF) 2 signaling pathway. This pathway protects cortical neurons against excitotoxicity that occurs in neurodegenerative diseases such as Alzheimer’s disease. Dolga was able to restate Lovastatin’s protection on cortical neurons, on her current in vivo animal study, and reaffirm that the neuroprotective effect of Lovastatin is dependent on the activation of other factors in the TNF pathway. Her findings strongly suggest that Lovastatin may be a promising guide towards improving neurodegenerative diseases. However, more studies need to be performed in order to be certain of statins’ benefits against Alzheimer’s disease.
More details about this study can be found in the June issue of The Journal of Alzheimer’s Disease.
Nova Southeastern University College of Pharmacy
According to the Alzheimer’s Association, Alzheimer’s disease is the seventh leading cause of death in the United States and affects more than 5 million Americans. This neurodegenerative disease targets brain cells causing irreversible damage and neuronal cell death, which results in severe memory impairment and radical changes in behavior. The Alzheimer’s Association also states that it is the most common form of dementia, accounting for 50 to 70 percent of dementia cases. Currently, this eventually fatal disease has no cure, and only symptomatic treatment and supportive care are offered to these patients in order to improve their quality of life. Consequently, it comes as no surprise that the struggle to find a way to reverse or eradicate this disease is crucial.
Recent promising studies show that statins, a class of commonly used cholesterol lowering drugs, may help protect brain cells against excitotoxicity, which consists on overstimulation of nerve cells, eventually leading to cell death. Overstimulation is the leading cause of degeneration of nerve cells in Alzheimer’s patients.
Lovastatin was the cholesterol reducing statin used in animal studies done by Amalia Dolga, PhD and her colleagues at the University of Groningen in the Netherlands. Her study showed that besides reducing cholesterol, Lovastatin was able to protect nerve cells against damage caused by overstimulation. By avoiding damage on nerve cells we can extend their memory capacity, avoid their deterioration and cell death caused by Alzheimer’s disease.
On her previous in vitro Lovastatin study, Dolga and colleagues were able to demonstrate this dug’s neuroprotection ability through the activation of the tumor necrosis factor (TNF) 2 signaling pathway. This pathway protects cortical neurons against excitotoxicity that occurs in neurodegenerative diseases such as Alzheimer’s disease. Dolga was able to restate Lovastatin’s protection on cortical neurons, on her current in vivo animal study, and reaffirm that the neuroprotective effect of Lovastatin is dependent on the activation of other factors in the TNF pathway. Her findings strongly suggest that Lovastatin may be a promising guide towards improving neurodegenerative diseases. However, more studies need to be performed in order to be certain of statins’ benefits against Alzheimer’s disease.
More details about this study can be found in the June issue of The Journal of Alzheimer’s Disease.
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