Hydroxycut products are dietary supplements that are marketed for weight-loss, as fat burners, as energy-enhancers, as low carb diet aids, and for water loss under the Lovate and MuscleTech brand names. The FDA is warning consumers to immediately stop using Hydroxycut products by Lovate Health Sciences Inc., of Oakville, Ontario and distributed by Lovate Health Sciences USA Inc. of Blasdell, N.Y. Some Hydroxycut products are associated with a number of serious liver injuries. Lovate has agreed to recall Hydroxycut products from the market. The FDA has received 23 reports of serious health problems ranging from jaundice and elevated liver enzymes, an indicator of potential liver injury, to liver damage requiring liver transplant. One death due to liver failure has been reported to the FDA. Other health problems reported include seizures; cardiovascular disorders; and rhabdomyolysis, a type of muscle damage that can lead to other serious health problems such as kidney failure. Liver injury, although rare, was reported by patients at the doses of Hydroxycut recommended on the bottle. Symptoms of liver injury include jaundice (yellowing of the skin or whites of the eyes) and brown urine. Other symptoms include nausea, vomiting, light-colored stools, excessive fatigue, weakness, stomach or abdominal pain, itching, and loss of appetite. The list of products being recalled by Lovate currently includes:
Hydroxycut Regular Rapid Release Caplets
Hydroxycut Caffeine-Free Rapid Release Caplets
Hydroxycut Hardcore Liquid Caplets
Hydroxycut Max Liquid Caplets
Hydroxycut Regular Drink Packets
Hydroxycut Caffeine-Free Drink Packets
Hydroxycut Hardcore Drink Packets (Ignition Stix)
Hydroxycut Max Drink Packets
Hydroxycut Liquid Shots
Hydroxycut Hardcore RTDs (Ready-to-Drink)
Hydroxycut Max Aqua Shed
Hydroxycut Carb Control
Although the FDA has not received reports of serious liver-related adverse reactions for all Hydroxycut products, Lovate has agreed to recall all the products listed above. Hydroxycut Cleanse and Hoodia products are not affected by the recall. Consumers who have any of the products involved in the recall are advised to stop using them and to return them to the place of purchase. The agency has not yet determined which ingredients, dosages, or other health-related factors may be associated with risks related to these Hydroxycut products. The products contain a variety of ingredients and herbal extracts. Health care professionals and consumers are encouraged to report serious adverse events (side effects) or product quality problems with the use of these products to the FDA’s MedWatch Adverse Event Reporting program online, by regular mail, fax or phone.
Influenza, commonly referred to as the flu, is an infectious disease caused by RNA viruses of the family Orthomyxoviridae, that affects birds and mammals. The name influenza comes from the Italian influenza, meaning “influence” (Latin: influentia). Influenza A virus strains are categorized according to two proteins found on the surface of the virus: hemagglutinin (H) and neuraminidase (N). The word influenza was first used in 1743 when it was adopted, with an anglicized pronunciation, during an outbreak of the disease in Europe. Archaic terms for influenza include epidemic catarrh, grippe. The symptoms of human influenza were clearly described by Hippocrates roughly 2,400 years ago. Since then, the virus has caused numerous pandemics. Historical data on influenza are difficult to interpret, because the symptoms can be similar to those of other diseases. The first convincing record of an influenza pandemic was of an outbreak in 1580, which began in Russia and spread to Europe via Africa. In Rome, over 8,000 people died, and several Spanish cities were almost wiped out. Pandemics continued sporadically throughout the 17th and 18th centuries, with the pandemic of 1830-1833 being particularly widespread, where it infected approximately a quarter of the people exposed. Some believe that the 1889-1890 Russian flu was caused by influenza A virus subtype H2N2, but the evidence is not conclusive. It is the earliest flu pandemic for which detailed records are available. In 1889, flu began in Russia and spread rapidly throughout Europe. It reached North America in December 1889 and spread to Latin America and Asia in February 1890. About 1 million people died in this pandemic. The most famous and lethal outbreak was the so-called Spanish flu pandemic (type A influenza, H1N1 subtype), which lasted from 1918 to 1919. It is not known exactly how many died, but estimates range from 20 to 100 million people. This pandemic has been described as “the greatest medical holocaust in history” and may have killed as many people as the Black Death. This huge death toll was caused by an extremely high infection rate of up to 50%, and the extreme severity of the symptoms was suspected to be caused by cytokine storms. Indeed, symptoms in 1918 were so unusual that initially influenza was misdiagnosed as dengue, cholera, or typhoid. One observer wrote, “One of the most striking of the complications was hemorrhage from mucous membranes, especially from the nose, stomach, and intestine. Bleeding from the ears and petechial hemorrhages in the skin also occurred.” The majority of deaths were from bacterial pneumonia, a secondary infection caused by influenza, but the virus also killed people directly, causing massive hemorrhages and edema in the lungs. The Spanish flu pandemic was truly global, spreading even to the Arctic and remote Pacific islands. The unusually severe disease killed between 2 and 20% of those infected, as opposed to the more usual flu epidemic mortality rate of 0.1%. Another unusual feature of this pandemic was that it mostly killed young adults, with 99% of pandemic influenza deaths occurring in people under 65, and more than half in young adults 20 to 40 years old. This is unusual since influenza is normally most deadly to the very young (under age 2) and the very old (over age 70). The total mortality of the 1918-1919 pandemic is not known, but it is estimated that 2.5% to 5% of the world’s population died. As many as 25 million may have died in the first 25 weeks. In contrast, HIV/AIDS has killed 25 million in its first 25 years. Later flu pandemics were not so devastating. They included the 1957 Asian Flu (type A, H2N2 strain) and the 1968 Hong Kong Flu (type A, H3N2 strain), but even these smaller outbreaks killed millions of people. In later pandemics antibiotics were available to control secondary infections and this may have helped reduce mortality compared to the Spanish Flu of 1918. The etiological cause of influenza, the Orthomyxoviridae family of viruses, was first discovered in pigs by Richard Shope in 1931. This discovery was shortly followed by the isolation of the virus from humans by a group headed by Patrick Laidlaw at the Medical Research Council of the United Kingdom in 1933. However, it was not until Wendell Stanley first crystallized tobacco mosaic virus in 1935 that the non-cellular nature of viruses was appreciated. The first significant step towards preventing influenza was the development in 1944 of a killed-virus vaccine for influenza by Thomas Francis, Jr. This built on work by Australian Frank Macfarlane Burnet, who showed that the virus lost virulence when it was cultured in fertilized hen’s eggs. Application of this observation by Francis allowed his group of researchers at the University of Michigan to develop the first influenza vaccine, with support from the U.S. Army. The Army was deeply involved in this research due to its experience of influenza in World War I, when thousands of troops died in a matter of months. Although there were major flu scares in the US: New Jersey in 1976 (with a strain of Swine Flu), worldwide in 1977 (with the Russian Flu), and in Hong Kong and other Asian countries in 1997 (with H5N1 avian influenza), there have been no major pandemics since the 1968 Hong Kong Flu. Immunity to previous pandemic influenza strains and vaccination may have limited the spread of the virus and may have helped prevent further pandemics.
Autism spectrum disorders (ASD) comprise a group of disorders with core symptoms that include social interaction problems, poor verbal and nonverbal communication and repetitive behaviors. These disorders range from severe (autism) to mild (Asperger’s syndrome), and in total affect some 1 in 150 American children, about three-quarters of whom are boys. Researchers theorize that the social parts of the brain are underdeveloped in ASD. Previous studies have suggested that autism is a developmental disorder resulting from abnormal connections in the brain. Three studies just reported (Nature: Wang K et al., and Glessner et al., published online April 28, 2009; Annals of Human Genetics: Ma D et al., published online April 28, 2009), include the most comprehensive study of autism genetics to date. These studies identify the most common and rare genetic factors that affect the risk of autism spectrum disorders. The results point to the importance of genes that are involved in forming and maintaining the connections between brain cells. All three studies were genome-wide association studies, which are undertaken to find clues about the causes of complex disorders. Typically, these studies involve scanning the genome – the entire set of DNA – for small differences between people who have a disorder and people who do not. The largest study, reported in Nature, involved more than 10,000 subjects, including individuals with ASD, their family members and other volunteers from across the U.S. Previous studies of twins with ASD, other children with ASD and their relatives provided evidence of a strong genetic contribution. Yet until now, only a few genetic risk factors had been identified, and most of those turned out to be rare, with unclear significance for ASD in the general population. In the largest study, several genetic variants were found that were commonly associated with ASD, all of them pointing to a spot between two genes on chromosome 5, called CDH9 and CDH10. Both genes encode cadherins – cell surface proteins that enable cells to adhere to each other. It was also found that a group of about 30 genes that encode cell adhesion proteins (including cadherins and neurexins) were more strongly associated with ASD than all other genes in their data set. In the developing brain, cell adhesion proteins enable neurons to migrate to the correct places and to connect with other neurons. The second study provides a striking confirmation that ASD is associated with variation near CDH9 and CDH10. Finally, a third study observed that in rare cases where those variations occurred, many tended to affect genes involved in cell adhesion. Other variations tended to affect genes involved in the ubiquitin-proteasome system, a cellular waste disposal system that probably affects the turnover of adhesion proteins at the cell surface. Previous, smaller genetic studies reported a connection between male-only autism and CNTNAP2, a type of neurexin. Together, the three new studies suggest that genetic differences in cell-to-cell adhesion could influence susceptibility to ASD on a large scale.
Promising results from a small study may offer hope for the treatment of multiple sclerosis (MS). Researchers from the University of California San Diego (UCSD) report dramatic improvement after treating MS patients with 1) ___ vascular fraction (SVF) stem cells from a patient’s own body fat. They say the SVF therapy can limit the body’s 2) ___ system reaction and promote the growth of new myelin. Myelin is the fatty “insulation” on axons in the brain, which breaks down in patients with MS. “None of the presently available MS treatments selectively inhibit the immune attack against the nervous system, nor do they stimulate 3) ___ of previously damaged tissue, but SVF cells may fill this therapeutic gap” said Boris Minev, M.D., from the Division of Neurosurgery at UCSD. Only three patients were treated in the study, but all three showed dramatic results following treatment, including improved balance and coordination and increased energy. Frequent, painful 4) ___ had stopped. SOURCE: Non-Expanded Adipose Stromal Vascular Fraction Cell Therapy for Multiple Sclerosis. Journal of Translational Medicine, April 2009
1) stromal; 2) immune; 3) regeneration; 4) seizures
The optimal time for the initiation of antiretroviral therapy for asymptomatic patients with human immunodeficiency virus (HIV) infection is uncertain. As a result, a study published in the New England Journal of Medicine (2009;360:1815-1826) evaluated the time from diagnosis to treatment and its effect on survival. Two parallel analyses were conducted involving a total of 17,517 asymptomatic patients with HIV infection in the US and Canada who received medical care during the period from 1996 through 2005. None of the patients had undergone previous antiretroviral therapy. In each group, patients were stratified according to the CD4+ count (351 to 500 cells per cubic millimeter or >500 cells per cubic millimeter) at the initiation of antiretroviral therapy. In each group, the relative risk of death was compared for patients who initiated therapy when the CD4+ count was above each of the two thresholds of interest (early-therapy group) with that of patients who deferred therapy until the CD4+ count fell below these thresholds (deferred-therapy group). Results of the first analysis, which involved 8,362 patients, 2,084 (25%) initiated therapy at a CD4+ count of 351 to 500 cells per cubic millimeter, and 6,278 (75%) deferred therapy. After adjustment for calendar year, cohort of patients, and demographic and clinical characteristics, among patients in the deferred-therapy group there was an increase in the risk of death of 69%, as compared with that in the early-therapy group (relative risk in the deferred-therapy group, 1.69; P<0.001). In the second analysis involving 9,155 patients, 2,220 (24%) initiated therapy at a CD4+ count of more than 500 cells per cubic millimeter and 6,935 (76%) deferred therapy. Among patients in the deferred-therapy group, there was an increase in the risk of death of 94% (relative risk, 1.94; P<0.001). According to the authors, the early initiation of antiretroviral therapy before the CD4+ count fell below two prespecified thresholds significantly improved survival, as compared with deferred therapy.
Differences in Control of Cardiovascular Disease and Diabetes by Race, Ethnicity, and Education: U.S. Trends From 1999 to 2006 and Effects of Medicare Coverage
It has been hypothesized that efforts to improve the care of cardiovascular disease and diabetes or to expand insurance coverage for adults with these conditions may reduce differences in clinical outcomes. As a result, a study published in the Annals of Internal Medicine (2009;150: 505-515), was performed to assess recent national trends in disease control, trends in sociodemographic differences in control, and changes in sociodemographic differences after age 65 years associated with near-universal Medicare The results were derived from data obtained from the National Health and Nutrition Examination Survey, 1999 to 2006. Study participants were adults age 40 to 85 years with relevant clinical conditions. Measurements included: 1) blood pressure control (<140/90 mm Hg) and mean systolic blood pressure among adults with hypertension (n = 4,521); glycemic control (hemoglobin A1c levels <7.0%) and mean hemoglobin A1c levels among those with diabetes (n = 1,733); and total cholesterol level control (<5.2 mmol/L [<200 mg/dL]) and mean total cholesterol levels among those with coronary heart disease, stroke, or diabetes (n = 2,928). Temporal trends in these measures were compared by race, ethnicity, and education, and sociodemographic differences were compared above and below eligibility for Medicare at age 65 years. Results showed that disease control improved significantly between 1999 and 2006 for all 6 measures (P < 0.001). These trends did not differ by race or ethnicity or by education (P 0.185 for group-time interactions), except that white-Hispanic differences in glycemic control widened (P = 0.042). Black-white differences in systolic blood pressure were smaller among adults age 65 to 85 years than among adults age 40 to 64 years (reduction in difference, 4.2 mm Hg; P = 0.009). Black-white differences in hemoglobin A1c levels were also smaller after age 65 years (reduction in difference, 0.7%; P = 0.005), as were Hispanic-white differences (reduction in difference, 0.7%; P = 0.007) and differences between less and more educated adults (reduction in difference, 0.5%; P = 0.033). According to the authors, control of blood pressure and glucose and cholesterol levels has improved since 1999 for adults with cardiovascular disease and diabetes, but racial, ethnic, or socioeconomic differences have not narrowed significantly. Medicare coverage after age 65 years is associated with reductions in these differences.