Hidden Health Science

Archive for the ‘Medical Alternatives’ Category

Abstract

The study was conducted to investigate the platelet increasing property of Carica papaya leaves juice (CPLJ) in patients with dengue fever (DF). An open labeled randomized controlled trial was carried out on 228 patients with DF and dengue haemorrhagic fever (DHF). Approximately half the patients received the juice, for 3 consecutive days while the others remained as controls and received the standard management. Their full blood count was monitored 8 hours for 48 hours. Gene expression studies were conducted on the ALOX 12 and PTAFR genes. The mean increase in platelet counts were compared in both groups using repeated measure ANCOVA. There was a significant increase in mean platelet count observed in the intervention group (P < 0.001) but not in the control group 40 hours since the first dose of CPLJ. Comparison of mean platelet count between intervention and control group showed that mean platelet count in intervention group was significantly higher than control group after 40 and 48 hours of admission (P < 0.01). The ALOX 12 (FC??=??15.00) and PTAFR (FC??=??13.42) genes were highly expressed among those on the juice. It was concluded that CPLJ does significantly increase the platelet count in patients with DF and DHF.

Introduction

Malaysia is blessed with 12000 species of flowering plants of which 1300 have medicinal properties [1]. There is a rapidly growing response to the use of medicinal plants by the Malaysian population. WHO estimates that in many countries 80% of the rural patients seek alternative treatment using medicinal plants.

Carica papaya is a member of the Caricaceae and is a dicotyledonous, polygamous, and diploid species [2]. It originated from Southern Mexico, Central America, and the northern part of South America. It is now cultivated in many tropical countries such as Bangladesh, India, Indonesia, Sri Lanka, the Philippines, and the West Indies including Malaysia. Malaysia is known to be one of the top 5 papaya exporting countries [3]. The papaya fruit is globally consumed either in its fresh form or the form of juices, jams, and crystallized dry fruit [4]. The ripe fruit is said to be a rich source of vitamin A, C, and calcium [5]. There are many commercial products derived from the different parts of the C. papaya plant, the most prominent being papain and chymopapain, which is produced from the latex of the young fruit, stem, and the leaves. C. papaya leaves have been used in folk medicine for centuries. Recent studies have shown its beneficial effect as an anti-inflammatory agent [6], for its wound healing properties [7], antitumour as well as immune-modulatory effects [8] and as an antioxidant [9]. A toxicity study (acute, subacute, and chronic toxicity) conducted on Sprague Dawley rats administered with Carica papaya leaves juice (CPLJ) of the sekaki variant revealed that it was safe for oral consumption [10].

Dengue is an arthropod-borne viral disease carried by Aedes aegypti as the vector, caused by 4 possible viral serotypes, namely, serotype 1, 2, 3, and 4 of the Flaviviridae family. In Malaysia, dengue cases have been on the rise since 2002. Total of 18,371 cases of dengue fever (DF) and dengue haemorrhagic fever (DHF) were reported last year and had claimed 33 lives  in the same year [11]. There is no specific antiviral drug available for the treatment of dengue infection. Infected patients receive supportive management with fluids, blood and blood, products complying to the Ministry of Health Clinical Practice Guidelines (CPGs) on Management of Dengue, 2010. Each episode of infection is known to induce a life-long protective immunity to the homologous serotype but confers only partial and transient protection against subsequent infection by the other serotypes. Secondary infection is a major risk factor for DHF possibly due to antibody-dependent enhancement. A patient with dengue fever presents typically with fever, headache, and rash known as the dengue triad. There are many other nonspecific signs and symptoms associated with DF and patient can progress to DHF and typically manifests as abdominal pain, bleeding, and even circulatory collapse. The clinical course of dengue has an abrupt onset followed by three phases, namely, the febrile phase, the critical phase and the recovery phase. It is during the critical phase that thrombocytopaenia, characterized by a decrease in platelet count below 100 000?per?mm3 from the baseline and haemoconcentration, characterized by an increase of haematocrit by 20% or more, is  detectable before the subsidence of fever and the onset of shock [12].

Certain genes have been shown to influence platelet production and platelet aggregation, namely, the Arachidonate 12-lipoxygenase (ALOX 12) also known as the Platelet-type Lipoxygenase as well as the Platelet-Activating Factor Receptor (PTAFR). An increase in activity of these genes is required for platelet production and activation. The ALOX 12 gene is strongly expressed in megakaryocytes and has been known to be responsible for the 12-Hydroxyeicosatetraenoic acid (12-HETE) production of platelets [13]. The PTAFR gene was been found to be expressed in megakaryocytes indicating that it could be a precursor for platelet production in addition to its well known role in platelet aggregation [14].

Safety studies based on OECD guidelines for acute, subacute, and chronic toxicity were conducted on C. papaya extract and showed that it was found to be safe for human consumption [10]. The present study was conducted to determine and investigate the traditional claim that CPLJ increases the platelet count in patients with DF and DHF.

Results

A total of 145 patients were recruited into the interventional group while 145 patients were recruited into the control group. At the end of the study, 111 patients from the interventional group and 117 controls were included in the statistical analysis. Sixty-two patients were excluded from the analysis as 38 patients were lost to followup and 24 patients had incomplete data (missing results due to sample rejection).

Table 1 shows demographic characteristics and baseline biochemistry investigation of respondents by treatment. In terms of dengue status, all patients recruited had either dengue NS1 or IgM or both detected, while the percentage distribution of the dengue serotypes among them was DEN1 (30.4%), DEN2 (28.4%), DEN 3 (20.6%), and DEN 4 (20.6%). Hence, all serotypes were well represented in the study.

Table 2 presents the multiple comparisons of mean platelet count 8 hours after admission with mean platelet count at 16, 24, 32, 40, and 48 hours after admission for interventional and control group Multiple paired t-test was conducted to demonstrate if there was any significant difference in mean platelet count for each comparison. Hence, Bonferroni correction was applied to reduce the possibility of rejecting a true null hypothesis (committing a type 1 error). Based on the number of patients recruited with complete data (111 patients from the intervention group and 117 control), the power of study was 87.0% (standard deviation of platelet count of 40,000, type I error probability of 0.01, and the true difference in mean platelet count of 20,000 between the intervention and control group). Overall, there was a significant increase in mean platelet count over 40 hours in both groups (Wilk’s Lambda = 0.939, P=0.015, effect size = 0.06, and power = 84.0%) after adjusting for age. Further analysis by using multiple paired t-test on each of the groups showed that there was a significant increase in mean platelet count at 40 hours compared to 8 hours after intervention in the intervention group (t=-4.256, P <= 0.001) but not in the control group (t=-2.399, P=0.018) after adjustment of Bonferroni correction (P=0.05/5 = 0.01).

Read the study at Hindawi.

from Clinchem

• Received for publication August 5, 2012.
• Accepted for publication September 21, 2012.

• © 2012 The American Association for Clinical Chemistry

Cannabis sativa plant (Photo credit: Wikipedia)

A new study published in the Journal of OFOG-E-DANESH at the Gonabad University of Medical Sciences and Health Services in Iran has found that cannabis sativa, as an alcoholic extract, can  work as a neuroprotective agent to slow or halt the progression of  neural system disorders as a result of hyperglycemia.

Neuroprotective effects of Cannabis sativa alcoholic extract against spinal alpha motoneurons degeneration in male type II diabetic rats

Article abstract:
Aims: Diabetic neourophaty is one of the long-term normal results of diabetes. According to anti-tumor, anti-diabetic and anti-oxidant effects of Cannabis sativa, the aim of this research was to investigate the effect of Cannabis sativa alcoholic extract on Alpha motoneurons degeneration after sciatic nerve compression in diabetic rats.

Methods: This experimental laboratorial research was performed in 30 Wistar male rats with the weight of 300 to 350g in 5 “control”, “compression” , “compression+diabetes”, “compression+diabetes+treatment with 25mg/kg alcoholic extract of Cannabis sativa seed” and “compression+diabetes+treatment with 50mg/kg alcoholic extract of Cannabis sativa seed” groups. After preparing the alcoholic extract of Cannabis sativa seed, 18 rats were undergone diabetes induction and 24 rats were taken compression surgery. Spinal cord samples were taken from all 30 rats. Data was analyzed by Minitab 14 software and ANOVA test. Results: Neuronal density of “compression” group () was decreased significantly in comparison with “control” group (). There was a significant difference between neuronal density of “compression” group and “compression+diabetes” () group. Comparison of neuronal density between “compression+diabetes” group and rats treated with 25 and 50mg/kg doses of ethanolic extracts showed significant differences; in both treated groups, the neuronal density was increased compare to “compression” and “compression+diabetic” groups.

Conclusion: Using alcoholic extract of Cannabis sativa as a neuroprotective agent can prevent the progression of neural system disorders as a result of hyperglycemia.

Government-funded study proves cannabis shrinks tumors.

Abstract

Cannabinoids, the active components of Cannabis sativa L., act in the body by mimicking endogenous substances–the endocannabinoids–that activate specific cell surface receptors. Cannabinoids exert various palliative effects in cancer patients. In addition, cannabinoids inhibit the growth of different types of tumor cells, including glioma cells, in laboratory animals. They do so by modulating key cell signaling pathways, mostly the endoplasmic reticulum stress response, thereby inducing antitumoral actions such as the apoptotic death of tumor cells and the inhibition of tumor angiogenesis. Of interest, cannabinoids seem to be selective antitumoral compounds, as they kill glioma cells, but not their non-transformed astroglial counterparts. On the basis of these preclinical findings, a pilot clinical study of Delta(9)-tetrahydrocannabinol (THC) in patients with recurrent glioblastoma multiforme has been recently run. The good safety profile of THC, together with its possible growth-inhibiting action on tumor cells, justifies the setting up of future trials aimed at evaluating the potential antitumoral activity of cannabinoids.

Read it here.

NORML

The oral administration of cannabis extracts significantly reduces muscle stiffness in patients with multiple sclerosis (MS), according to just published clinical trial data published in the Journal of Neurology, Neurosurgery & Psychiatry.

Investigators at the University of Plymouth, Clinical Neurology Research Group, in the United Kingdom assessed the use of cannabinoids versus placebo in 279 subjects with MS over a twelve-week period. Cannabis extracts in the study contained standardized doses of THC and cannabidiol (CBD), a non-psychoactive constituent in cannabis, contained in a soft, gelatin capsule.

Investigators reported that oral cannabis extracts were “superior” over placebo in the treatment of MS-associated muscle stiffness and pain.

Authors concluded: “Treatment with standardized oral extract of cannabis sativa relieved muscle stiffness. The proportion of participants experiencing relief was almost twice as large in the cannabis extract group as in the placebo group. … Effective pain relief is also achieved by cannabis extracts, especially in patients with a high baseline pain score. Our findings suggest that standardized cannabis extracts can be clinically useful in treating the highly complex phenomenon of spasticity in MS.”

In May, clinical trial data published in the Journal of the Canadian Medical Association reported that cannabis inhalation significantly mitigates spasticity and pain in patients with treatment-resistant multiple sclerosis.

Separate clinical trials assessing the administration of oral cannabis extracts on patients with MS have indicated that cannabinoids can alleviate symptoms of the disease long-term and may also act in ways to mitigate MS progression. Sativex, an oral spray containing plant cannabis extracts, is presently legal by prescription to treat MS-related symptoms in over a dozen countries, including Canada, Germany, Great Britain, New Zealand, and Spain. Nonetheless, the National MS Society of the United States shares little enthusiasm for cannabis as a potential treatment for multiple sclerosis, stating, “Studies completed thus far have not provided convincing evidence that marijuana or its derivatives provide substantiated benefits for symptoms of MS.”

Full text of the study, “Multiple Sclerosis and Extract of Cannabis: results of the MUSEC trial,” appears in the Journal of Neurology, Neurosurgery & Psychiatry. 

by Dr. Mercola

When I first read that genetically modified humans have already been born, I could hardly believe it. However, further research into this story featured in the UK’s Daily Mail¹proved it to be true. They’ve really done it… they’ve created humans that nature could never allow for, and it’s anyone’s guess as to what will happen next.

Even more shocking was the discovery that this is actually old news!

The Daily Mail article was not dated, and upon investigation, the experiments cited actually took place over a decade ago; the study announcing their successful birth was published in 2001².

While I typically comment on recent findings and health related news, in this case I will make an exception, because I think many of you may be as surprised by this information as I was. I do not propose to have any answers here as this is out of my scope of expertise.

At best, I hope I can stir you to ponder the implications of this type of genetic engineering, and I invite you to share your perspective in the vital votes’ comment section below. As reported in the featured article:

“The disclosure that 30 healthy babies were born after a series of experiments in the United States provoked another furious debate about ethics… Fifteen of the children were born… as a result of one experimental program at the Institute for Reproductive Medicine and Science of St Barnabas in New Jersey.

The babies were born to women who had problems conceiving. Extra genes from a female donor were inserted into their eggs before they were fertilized in an attempt to enable them to conceive.

Genetic fingerprint tests on two one-year- old children confirm that they have inherited DNA from three adults—two women and one man.”

Human Germline Now Altered… What Happens Next?

Today, these children are in their early teens, and while the original study claims that this was “the first case of human germline genetic modification resulting in normal healthy children,” later reports put such claims of absolute success in dispute. Still, back in 2001, the authors seemed to think they had it all under control, stating:

“These are the first reported cases of germline mtDNA genetic modification which have led to the inheritance of two mtDNA populations in the children resulting from ooplasmic transplantation. These mtDNA fingerprints demonstrate that the transferred mitochondria can be replicated and maintained in the offspring, therefore being a genetic modification without potentially altering mitochondrial function.”

It’s relevant to understand that these children have inherited extra genes—that of TWO women and one man—and will be able to pass this extra set of genetic traits to their own offspring. One of the most shocking considerations here is that this was done—repeatedly—even though no one knows what the ramifications of having the genetic traits of three parents might be for the individual, or for their subsequent offspring.

Based on what I’ve learned about the genetic engineering of plants, I’m inclined to say the ramifications could potentially be vast, dire, and completely unexpected.

As a general, broad-strokes rule, it seems few scientists fond of gene-tinkering have a well-rounded or holistic view of living organisms, opting instead to view the human body as a machine. And as demonstrated with the multi-varied problems that have arisen from genetically engineered foods—from the development of superweeds and superpests, to the creation of a never-before-seen organism now linked to miscarriage and infertility—such a view is bound to lead you to the wrong conclusions…

Read more at this link.

by Paul Armentano, NORML

The use of cannabis and cannabinoids appears to mitigate symptoms associated with post-traumatic stress disorder (PTSD), according to a new review of clinical and preclinical evidence published online in the scientific journal Drug Testing and Analysis.

An international team of investigators from Germany, the United States, and the United Kingdom reported that the use of cannabis to “dramatically reduced” PTSD symptoms in a single 19-year-old male patient.

Authors reported: “In the case report presented in this review, the patient displayed a grave pathology involving anxiety, dissociation and heavy flashbacks as a consequence of PTSD. … The patient stated that he found cannabis more useful than lorazepam. … It is evident from the case history that the patient experienced reduced stress, less involvement with flashbacks and a significant decrease of anxiety.”

Authors further cited “accumulating clinical and preclinical evidence that cannabinoids may mitigate some major symptoms associated with PTSD.”

They concluded: “Cannabis may dampen the strength or emotional impact of traumatic memories through synergistic mechanisms that might make it easier for people with PTSD to rest or sleep and to feel less anxious and less involved with flashback memories. … Evidence is increasingly accumulating that cannabinoids might play a role in fear extinction and anti-depressive effects. It is concluded that further studies are warranted in order to evaluate the therapeutic potential of cannabinoids in PTSD.”

Last year, administrators at the United States Department of Health and Human Services, National Institute on Drug Abuse (NIDA) blocked investigators at the University of Arizona at Phoenix from conducting an FDA-approved, placebo-controlled clinical trial to evaluate the use of cannabis in 50 patients with PTSD.

Under federal law, any clinical trial evaluations involving cannabis must receive NIDA approval because the agency is the only source of legal cannabis for FDA-approved research purposes. In 2010, a spokesperson for the agency told The New York Times: “[O]ur focus is primarily on the negative consequences of marijuana use. We generally do not fund research focused on the potential beneficial medical effects of marijuana.”

by Paul Armentano, NORML

The legalization of cannabis for therapeutic purposes is not associated with increases in the use of marijuana or other illicit substances among adolescents, according to discussion paper commissioned by the Institute for the Study of Labor (IZA) in Germany.

Economists from Montana State University, the University of Oregon, and the University of Colorado, Denver examined the relationship between state medical cannabis laws and marijuana consumption among high school students. Authors analyzed data from the national and state Youth Risky Behavior Surveys (YRBS) for the years 1993 through 2009 – during which time 13 states enacted law allowing for the production and use of cannabis for medicinal purposes.

The national YRBS is conducted biennially by the Centers for Disease Control and Prevention (CDC) and is a nationally representative sample of U.S. high school students.

Authors reported that the survey data provides no evidence that the enactment of medical cannabis legalization adversely impacted adolescents’ drug consumption. They concluded: “Our results are not consistent with the hypothesis that the legalization of medical marijuana caused an increase in the use of marijuana and other substances among high school students. … Our results suggest that the legalization of medical marijuana was not accompanied by increases in the use of marijuana or other substances such as alcohol and cocaine among high school students. Interestingly, several of our estimates suggest that marijuana use actually declined with the passage of medical marijuana laws.”

A 2012 study by researchers at McGill University in Montreal and published in the journal Annals of Epidemiology previously reported similar findings, concluding: “[P]assing MMLs (medical marijuana laws) decreased past-month use among adolescents … and had no discernible effect on the perceived riskiness of monthly use. … [These] estimates suggest that reported adolescent marijuana use may actually decrease following the passing of medical marijuana laws.”

Previous investigations by research teams at Brown University in 2011 and Texas A&M in 2007 made similar determinations, concluding, “[C]onsistent with other studies of the liberalization of cannabis laws, medical cannabis laws do not appear to increase use of the drug.”

The findings of these studies contradict public statements made by Drug Czar Gil Kerlikowske and other medical cannabis opponents, who in recent years have repeatedly alleged that the passage of medical cannabis laws is directly responsible for higher levels of self-reported marijuana consumption among US teenagers.

Full text of the study, “Medical Marijuana Laws and Teen Marijuana Use,” is available online at: http://ftp.iza.org/dp6592.pdf.

Scientists have discovered that they can dramatically increase the life span of mice with progeria (premature ageing disease) and heart disease (caused by Emery-Dreifuss muscular dystrophy) by reducing levels of a protein called SUN1. This research was done by A*STAR’s Institute of Medical Biology (IMB) in collaboration with their partners at the National Institute of Allergy and Infectious Diseases in the United States and the Institute of Cellular and System Medicine in Taiwan. Their findingswere published in the prestigious scientific journal, Cell, on 27th April 2012 and provide an exciting lead into developing new methods to treat premature aging and heart disease.

Children with progeria suffer symptoms of premature ageing and mostly die in their early teens from either heart attack or stroke. Individuals with Emery-Dreifuss muscular dystrophy (AD-EDMD) suffer from muscle wasting and cardiomyopathy, a type of heart disease that weakens and enlarges the heart muscle making it harder for the heart to pump blood and deliver it to the rest of the body leading to heart failure. Both diseases are caused by mutations in Lamin A, a protein in the membrane surrounding a cell’s nucleus which provides mechanical support to the nucleus. SUN1 is a protein also found in the inner nuclear membrane, but there have been no previous studies to show how SUN1 interacts with the Lamin proteins.

The scientists wanted to investigate if SUN1 had any involvement in diseases caused by mutations in Lamin A, so they inactivated SUN1 in mouse models developed for progeria and AD-EDMD. These mouse models for progeria and AD-EDMD usually thrive poorly and have markedly short life spans as they die from premature ageing and heart failure respectively. However, by inactivating SUN1 and reducing SUN1 levels in these mouse models, the scientists observed that the life spans of the mouse models for progeria and AD-EDMD doubled and tripled respectively.

“We actually expected that knocking out Sun1 in these mouse models would worsen their conditions and cause them to die faster but surprisingly we observed the opposite. This is the first time that Sun1 protein has been implicated in diseases linked to Lamin A and it is exciting how basic research has led to a discovery that can potentially have significant impact on us,” said Rafidah Abdul Mutalif, who is pursuing her PhD at IMB and one of the main authors of this paper.

Prof. Colin Stewart, Principle Investigator at IMB, said, “Notably, the heart muscle of the mice was restored to near normal function and cardiac function improved when the levels of SUN1 were reduced. Mutations in Lamin A are frequently reported as a cause of heart disease and especially within a groupof hereditary cardiomyopathies. This opens up a possibility that from these observations, reduction in SUN1 maybe of therapeutic use for other forms of heart disease. We are very excited about this discovery and look forward to further pursuing thislead which could potentially lead to development of new treatments for heart diseases.”

The research findings described in this news release can be found in the 27 Apr issue of Cell, Chen, C-Y et al 2012 as Accumulation of the Inner Nuclear Envelope Protein Sun1 Is Pathogenic in Progeric and Dystrophic Laminopathies Cell 149.

Read more at Nano Patents and Innovations